Intelligent Design

Consider the opossum: the evidence for common descent

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Remarkably, the recent spate of articles over at Evolution News and Views (see here, here and here) attacking the claim that vitellogenin pseudogenes in humans provide scientific evidence for common descent, all missed the point that Professor Dennis Venema was making, which was not about the existence of pseudogenes, but about the spatial pattern in the genes. The pattern is strikingly clear if we compare chickens with opossums. And since humans belong to the same class as opossums (namely, mammals), any scientific evidence that chickens and opossums have a common ancestor also counts as strong prima facie evidence that chickens and humans have one.

I’d like to acknowledge at the outset the kind assistance given to me by Professor S. Joshua Swamidass, without whose thoughtful advice this post would not have been possible. My expertise lies in the field of philosophy rather than biology. I have endeavored to be as careful as possible in stating the scientific case for common descent; however, if there are any (unintentional) scientific errors in this post, then I take full responsibility for them. I would also like to make it clear that despite my criticisms (in this post) of Dr. Jeffrey Tomkins and the authors of the three articles written in response to Professor Venema over at Evolution News and Views, I do not wish to impugn their personal and scientific integrity.

Professor Venema’s five-part series on Vitellogenin and Common Ancestry is titled, Vitellogenin and Common Ancestry: Does BioLogos have egg on its face? (February 11, 2016). Venema responds to criticisms made by creationist Dr. Jeffrey Tomkins in sections three and four.

As I see it, the recent articles written in response to Professor Venema over at Evolution News and Views suffer from seven fundamental flaws:

(i) ignoring the main evidence for common descent;

(ii) faulty statistics: misconstruing the evidence for common descent;

(iii) changing the definitions of key terms (e.g. “pseudogene”);

(iv) obscuring the issue, by appealing to possible functions of pseudogenes, as an explanation for their presence in both chickens and mammals;

(v) engaging in wild speculation which goes far beyond the available evidence;

(vi) reliance on flawed analogies; and

(vii) theologizing the argument for common descent.

Let’s look at each in turn.

1. Ignoring the main evidence for common descent

Let me begin with a short definition. The term synteny simply refers to the condition of two or more genes, which may or may not be linked, being located on the same chromosome. The term shared synteny refers to the fact that in different species of animals, the spatial arrangement of genes on a chromosome is often conserved: not only do we find the same genes, but we find them in the same order along the same chromosome. In a nutshell, Professor Venema’s argument is that shared synteny is best explained by the hypothesis of common ancestry.

The evidence for the common descent of egg-laying birds (such as the chicken) and mammals is handily summarized in the third article of Professor Venema’s five-part series, which is titled, Vitellogenin and Common Ancestry: Reading Tomkins:

Evolutionarily speaking, the observed shared synteny for the VIT regions in humans and chickens makes a prediction about what we should find in other mammals. Since the last common ancestral population of humans and chickens lived prior to the evolution of all mammals, we would expect to (at least potentially) find these regions in any other mammal we care to sequence – with the understanding that these sequences might be missing if they have been lost in a particular lineage…

The researchers thus looked for VIT genes in a diverse number of mammals, and, not surprisingly, found them in the same arrangement as seen in chickens and humans. One example comes from a marsupial mammal – the opossum. Just like for humans, the opossum VIT genes are riddled with mutations that prevent them from being translated into proteins. Despite those mutations, however, enough VIT gene remnants and their non-gene flanking sequences remain in opossums to easily identify them – nested between the same functional genes we see in humans and chickens. In fact, in opossums, more of the VIT2 and VIT3 sequences remain than in the human genome, and more of the DNA flanking VIT1 remains the same.

These findings, then, match what common ancestry predicts if indeed humans, chickens, and opossums share a common ancestral population deep in the past. Opossums, since they do not lay eggs, do not require VIT genes any more than placental mammals like humans do. Nonetheless, they too have remnants of these genes in the exact places in their genomes that common ancestry would predict. Moreover, the researchers found that several other placental and marsupial mammals also have VIT pseudogenes. As you might expect, however, egg-laying mammals (such as the platypus) retain a functional VIT gene that they use to perform bulk yolk transfer to their embryos.

In summary, what we see is a broad pattern of evidence that supports the hypothesis that placental and marsupial mammals share common ancestral populations with egg-laying mammals, and more distantly, other egg-laying vertebrates such as birds…

The true “main evidence” for the remains of VIT genes in the human genome is as we have discussed: the overall match of sequences between placental / marsupial mammals and egg-laying organisms over large spans of DNA, including flanking regions. This is the evidence that needs to be addressed – and Tomkins does not even mention it, let alone address it. (Bolding mine – VJT.)

So, how did Professor Venema’s critics over at Evolution News and Views deal with this evidence? Amazingly, they almost completely ignored it.

Remarkably, the first Evolution News and Views post in response to Professor Venema, which is titled, Functional Pseuodogenes and Common Descent (May 23, 2016), made no mention of opossums or other mammals. It only mentioned chickens and human beings. The article quoted a single sentence from Professor Venema referring to shared synteny, but it failed to provide a definition of this term, let alone a discussion of its significance. In other words, it completely missed the point that Venema was making.

The final ENV response to Professor Venema, titled, Humans, Chickens, and the Vitellogenin Pseudogene — Summing Up (Evolution News and Views, May 25, 2016), was no better. It totally ignored the evidence from shared synteny, and it focused exclusively on humans and chickens, as it tried to make a case that there was no scientific evidence for common descent:

Let’s take a moment to summarize the results of our comments on the vitellogenin pseudogene and its meaning for the question of universal common ancestry. According to the data, the debate concerns six total genes supposedly shared by humans and chickens

Three of those genes (ELTD1, SSX2IP, CTBS) are functional in both humans and chickens. No evidence of pseudogenes — shared or otherwise — is there.

Two of those genes (VIT2, VIT3) are functional in chickens and non-functional in humans, but according to the data our colleague Dr. Gauger showed, they are hardly found in humans at all. Arguably, they aren’t there.

One of those genes — the supposed “vitegellenin (sic) pseudogene” (VIT1) — is functional in chickens, but according to Tomkins (2015) it is also part of a functional gene in humans. It may not be making egg yolk but it’s not a non-functional stretch of DNA. Indeed, as Ann Gauger notes, the sequence alignment between the human and chicken versions is very low, so it’s not clear if they are the same gene.

Thus the relevant data yield the following conclusion: When we look at this block of six genes supposedly shared by humans and chickens, there are exactly zero non-functional pseudogenes shared between humans and chickens. (Bolding mine – VJT.)

The article says nothing about the spatial order of these genes, along the chromosome on which they are found.

Of the three articles written in response to Professor Venema over at Evolution News and Views, only Dr. Ann Gauger’s article, The Vitellogenin Pseudogene Story: Unequally Yoked (Evolution News and Views, May 24, 2016), discusses the significance of synteny, as well as the evidence from other mammals:

Synteny refers to how well chromosomal sequences from different species align with one another. Genes can be in the same general order and location between species, for example rat and mouse, or chimp and human. If they align well, evolutionists take the alignment as evidence for common ancestry. Sometimes, the gene sequences may be interrupted by deletions or insertions, and stop codons, which prevent the gene from making functional protein.

These “inactivated” genes are called pseudogenes, and are taken by evolutionists as further evidence for common descent. Their presence is explained as the remnants of once functional genes broken by mutation and no longer needed by the organism.

Egg-bearing animals use proteins called vitellogenins to transport nutrients in their egg yolk. Each vitellogenin is a very long complicated protein composed of many exons (stretches of DNA that must be copied into RNA and then spliced together into one contiguous piece before being translated into vitellogenin). An article by Dennis Venema lays out the supposed story: humans retain the remnants of DNA that used to code for egg yolk proteins called vitellogenins. Since humans don’t lay eggs, the argument goes, these “vitellogenin” pseudogenes, now long since mutated into near unrecognizability, must be inherited from common ancestors who did lay eggs. Venema claims that all three human “vitellogenin” pseudogenes, VIT1 through VIT3, show traces of sequence similarity to the functioning vitellogenin genes of the chicken…

This story is based on a 2008 paper by Brawand et al. that discusses yolk proteins in egg-laying animals and mammals. In that paper they identified the region of the chicken genome where vitellogenin genes are located, then found the similar regions in humans, dogs, and various marsupials and platypus, to see if vitellogenin pseudogenes could be found in the right syntenic neighborhoods. (Bolding mine – VJT.)

Dr. Gauger deserves credit for squarely addressing the evidence. She suggests that the shared synteny of the vitellogenin VIT1, VIT2 and VIT3 genes as well as the nearby ELTD1, SSX2IP and CTBS genes in chickens, marsupials and placental mammals could be due to some function which the vitellogenin gene fragments possess in mammals: “This similar order could be due to ancestry or functional reasons.” As we’ll see below, that won’t work – especially if the vitellogenin gene fragments are part of a long non-coding RNA, as is claimed by Dr. Jeffrey Tomkins (whose work Dr. Gauger cites). And as we’ll see in the following section, her claim that “evidence for vitellogenin pseudogenes in human and dog genomes… is very weak” is based on a flawed reading of the evidence. But at least Dr. Gauger fully realizes what the problem is, and she makes an honest attempt to address it.

Advantage: common descent

In a recent email communication, Professor S. Joshua Swamidass observes that the hypothesis of common descent readily explains two features of the data:

1. Why is the genetic signal stronger in the opossum (a marsupial mammal) than in human beings, who are placentals? The common descent model has an answer to this question: the various lines of mammals made the transition away from eggs at different times, so they inactivated their yolk genes at different times. How does the design model answer this question?

2. The identical spatial ordering of the genes (shared synteny) in different groups of animals. The common descent model can readily account for this fact: the shared ordering was inherited from a common ancestor. How does the design model explain it?

In short: every pattern that the common descent model explains is therefore evidence for common descent, or at least common descent plus design.

I’d like to ask Dr. Ann Gauger a question I posed to Dr. Cornelius Hunter in my previous post:

Do you accept that if hypothesis A readily explains an empirical fact F and hypothesis B does not, then F (taken by itself) constitutes scientific evidence for A over B? Or putting it another way, if a fact F is predicted by hypothesis A, and compatible with hypothesis B but not predicted by B, then do you agree that F constitutes scientific evidence for A over B? If not, why not?

To sum up: while the hypothesis of common design is consistent with the data, it fails to explain many of the patterns we see in the data. The hypothesis of common descent, on the other hand, explains these patterns; that is why we count them as evidence for common descent.

2. Faulty Statistics: Misconstruing the evidence for common descent

The second major flaw in the Evolution News and Views articles written in reply to Professor Dennis Venema’s five-part series on vitellogenin and common ancestry relates to the way in which they present the evidence for matching between different groups (taxa) of animals. The ENV articles are marred by the use of faulty statistics, coupled with a mis-reading of the 2008 paper by Brawand et al., which compares the vitellogenin data for various groups of animals.

(a) Getting the data on opossums wrong

Dr. Ann Gauger understates the evidence for the existence of vitellogenin pseudogenes in humans and other mammals. Here’s how she presents it in her article, The Vitellogenin Pseudogene Story: Unequally Yoked (Evolution News and Views, May 24, 2016):

Patches of sequence similarity to the chicken genome that might be interpreted as pseudogenes can be found in syntenic regions of marsupial genomes. Evidence for vitellogenin pseudogenes in human and dog genomes, on the other hand, is very weak. It is practically nonexistent for vitellogenin genes VIT2 and VIT3 (it is not statistically significant compared to the genomic background).

Dr. Gauger minimizes the significance of the evidence for vitellogenin pseudogenes VIT2 and VIT3 in marsupials (such as opossums) by saying that it “might be interpreted as pseudogenes.” In other words, she’s not even sure that opossums possess these pseudogenes. [NOTE: In a comment below, Origenes suggests that what Dr. Gauger is doing here is querying the common scientific definition of “pseudogene.” Even if this interpretation is correct, the comments in section 3 below would still apply – VJT.] However, if we examine the 2008 paper by Brawand et al. which she cites in her post, we find that the authors explicitly state that the matches between chickens and opossums are “real coding sequence matches” for the VIT1, VIT2 and VIT3 exons:

Figure 3. Genome Alignment (Dot Plot Representing SIM Alignments) of Opossum/Chicken Syntenic Regions VIT1-VIT3 Regions

The chain with the best cumulative score is shown. Alignment of flanking genes confirms the synteny of the aligned regions. The subsets of alignments corresponding to VIT exons of the best chain for all three regions have significantly higher scores than genomic background hits in the chain (p < 0.05, Mann-Whitney U test). This shows that VIT1-VIT3 exon matches in opossum represent nonrandom hits and thus correspond to real coding sequence matches.

In addition, we need to keep in mind the fact that the p-values which Dr. Gauger mentions in her article refer only to a single match. However, when one takes into account the fact that there are multiple matches in this region (a point on which I’ll elaborate below), it becomes apparent that the odds of these matches being in all the right places are very, very low. It isn’t enough to merely ask whether there is a statistically significant match between one sequence in a chicken and another sequence in a mammal (e.g. a human or an opossum). What we need to examine is the totality of the evidence.

It appears that Dr. Gauger has failed to fully grasp the strength of the genetic similarities between chickens and marsupial mammals, such as the opossum.

(b) Human vs. chicken: Do human beings have vitellogenin pseudogenes?

What about chickens versus human beings? Dr. Gauger writes:

Evidence for vitellogenin pseudogenes in human and dog genomes, on the other hand, is very weak. It is practically nonexistent for vitellogenin genes VIT2 and VIT3 (it is not statistically significant compared to the genomic background).

Regarding VIT2 and VIT3, Dr. Gauger is correct. Brawand et al. acknowledge: “The coding sequence matches for VIT2/3 may be too short to provide statistical significance or partially spurious.”

Dr. Gauger then proceeds to discuss the remaining VIT1 pseudogene:

The remaining gene, VIT1, has two patches of similarity in its putative former coding sequence, according to a supplemental figure in the paper.

The best of them is a patch 150 bases long (out of 42,637 total bases for the gene!) that has roughly 50 percent identity, by my estimation, and a few deletions to help make things match up. According to the authors, there is a 95 percent chance that the amount of similarity between VIT1 for humans and dogs, and the chicken VIT1, is not due to random chance — but that’s just at the borderline for statistical significance.

(i) Is the match statistically significant?

Professor Swamidass has two comments which are germane here. First, he points out that as a matter of standard practice, the data relating to similarity in the paper by Brawand et al. should be considered correct, unless proven otherwise. If Dr. Gauger thinks that the authors’ claims of similarity are doubtful, then I would invite her to show the exact DNA sequence she used, so that interested readers can perform a BLAST by themselves (there is a website for this), to verify both the match to the vitellogenin chicken gene and to the human sequence. This doesn’t resolve the issue of picking the right DNA sequence, but it is a start. Selecting the right parameters is important, too: if you use the wrong gapped parameter (a mistake Tomkins is notorious for making), then there will be discrepancies.

Second, in response to Dr. Gauger’s statement that the level of similarity between humans and chickens for the VIT1 pseudogene is “just at the borderline” for statistical significance, Professor Swamidass notes that the p-value quoted by Brawand et al. refers only to a single match. However, there are MULTIPLE matches in this region. When you combine this evidence with the fact that these matches are all in the right places (you can very approximately get this by just multiplying all the p-values together, or use the Fisher formula for a better number) the significance is very high, even for the human regions. The odds of this being due to chance are astronomically low.

(ii) “Only a 62% level of similarity”: Has Tomkins made another egregious error?

Dr. Gauger calculates that there is only about a 50% level of identity between human and chicken DNA for the 150 base pair fragment that she mentions. Only 50% identity? Hang on a minute! Dr. Jeffrey Tomkins calculates in his 2015 paper that the level of similarity is 62%, not 50%. So which is it? It would be very helpful if Dr. Gauger could oblige readers by submitting her BLAST test parameters.

If anything, Dr. Tomkins’ 62% figure is likely to be an underestimate, since he has, on previous occasions, made outlandish claims about low levels of similarity between human and chimp DNA, which turned out to be flat wrong. He once claimed that our DNA was less than 70% similar to the chimp’s – a claim that he had to retract when he discovered a computer bug in the BLAST algorithm. Then he claimed that the true figure was 88% – a claim that has since been eviscerated by computer programmer Glenn Williamson – see his recent blog article, Is 1% a Myth? Very briefly, the reason why Tomkins arrives at his figure of 88% is because of his use of the ungapped parameter in BLAST+. Instead of using only the best match when calculating the degree of similarity between human and chimp DNA sequences on focusing on that one, Tomkins takes the average of all the matches – good and bad alike – which brings his average down.

And how did Dr. Tomkins obtain that 62% similarity figure, anyway? Here’s what he says in the “Materials and Methods” section of his 2015 paper:

All genomic sequences were downloaded from the UCSC genome browser website using either the web interface or a Perl script written by author Tomkins. Pairwise DNA alignments were performed using the Geneious software package with the following parameters: global alignment with free end gaps, cost matrix of identity 1.0/0.0, gap open penalty of 3, and a gap extension penalty of 3. These parameters were employed due to the low homology of the sequences being aligned.

In other words, Dr. Tomkins admits that his choice of parameters assumed a low homology between the the relevant sequences in humans and chickens, at the outset. Hmmmm.

UPDATE: I get mail from Glenn Williamson

A few days ago, Glenn Williamson emailed me, saying that he had performed a quick BLAST. Here are the top four hits that he found:

8,620,1097,1,2789062,2788597,74.74,361,483,43500,3e-77
8,24111,24485,1,2758283,2757910,73.59,287,390,43500,1e-56
8,41677,42033,1,2715035,2714688,74.31,269,362,43500,1e-55
8,42618,42930,1,2714120,2713832,68.22,219,321,43500,3e-20

He added that he had carved out a smaller chunk of human chromosome 1 so that the blast would run quicker, and he advised anyone who was interested in checking his results to add 76,000,000 to the 5th and 6th fields.

Glenn Williamson also made the following quick observations:

· About 1,500 base pairs can be aligned with around 73% identity. That’s much more than the 150 base pairs that Tomkins chose to focus on. Readers will recall that Tomkins claimed only a 62% identity, even for this short segment.
· It’s in reverse.
· There is some basic synteny there (the four hits are in the right order).
· There are some repeats in the results, but they are relatively short (around 30 base pairs each).

I’ll leave it to readers to judge whether or not Dr. Tomkins has accurately presented the evidence for genetic similarity between humans and chickens in the vitellogenin pseudogene.

(iii) Does the overall level of similarity need to be high, anyway?

Finally, Professor Joshua Swamidass points out that the neutral theory of evolution predicts that the overall genetic similarity between chickens and humans would not be terribly high. After all, we’re talking about a 70-million-year-old gene here, so it’s hardly surprising that there would be a relatively weak match. In contrast, the relevant pseudogenes in the opossum are much more recent, and for that reason, they have a much stronger match. Common descent is capable of explaining this pattern; common design, by itself, cannot.

Summing up: Has Evolution News and Views presented the evidence accurately?

In short: Dr. Gauger’s assertion that the degree of similarity between VIT1 for humans and chickens is “just at the borderline for statistical significance” rests on a mis-reading of Brawand et al.’s 2008 paper. Regrettably, Dr. Gauger’s statement was bowdlerized in the final, anonymous Evolution News and Views article written in response to Venema, which baldly states: “as Ann Gauger notes, the sequence alignment between the human and chicken versions is very low, so it’s not clear if they are the same gene.” That, I am afraid, constitutes a serious mis-reading of the genetic data, and I’m not sure Dr. Gauger herself would endorse that way of summarizing the evidence.

3. Changing the definitions of key terms

In her article, The Vitellogenin Pseudogene Story: Unequally Yoked (Evolution News and Views, May 24, 2016), Dr. Ann Gauger begins by defining the term “pseudogene” in its standard sense:

Sometimes, … gene sequences may be interrupted by deletions or insertions, and stop codons, which prevent the gene from making functional protein.

These “inactivated” genes are called pseudogenes, and are taken by evolutionists as further evidence for common descent.

So far, so good. But later on in her article, Dr. Gauger approvingly cites a 2015 Answers in Genesis article by Dr. Jeffrey Tomkins, who declares that a gene fragment which turns out to have a function can no longer be called a pseudogene:

…the alleged vtg [vitellogenin] fragment in human is not a pseudogene remnant at all, but a functional enhancer element in the fifth intron of a “genomic address messenger” (GAM) gene… These combinatorial data clearly show that it is a functional enhancer element in a GAM gene expressed in the human brain — strongly challenging the idea that this sequence is an egg-laying pseudogene genomic fossil.

Swamidass comments that by citing this passage from Dr. Tomkins, which defines pseudo-genes in terms of their total lack of functionality, Dr. Gauger has effectively changed the definition of a pseudogene, setting aside the standard definition. Even if VTG in humans were a lncRNA with an important function, it would still be a pseudogene, because no protein is being expressed from it and it exhibits similarity to VTG in chickens, and is in the correct place in the genome.

To be fair, I should mention that Dr. Venema himself, back in 2010, wrote a post in which he inaccurately referred to pseudogenes as “non-functional” (see here and here). The Evolution News and Views article Functional Pseuodogenes and Common Descent (May 23, 2016), points out Dr. Venema’s errors, which were made six years ago. But as they say, two wrongs don’t make a right. And in his 2016 series, Vitellogenin and Common Ancestry: Does BioLogos have egg on its face?, Dr. Venema is very careful to state that pseudogenes can acquire new functions, after having lost their original ones:

The major problem with [Tomkins’] argument is that it subscribes to a false dichotomy: that this sequence is either a VIT1 pseudogene fragment or a functional part of another gene. From an evolutionary perspective, there is no issue with it being both. Part of evolutionary theory is the expectation that occasionally some sequences, after losing their original function, may come under natural selection to be repurposed to another function. The technical term for this process is exaptation, and many examples of it are known.

As we’ll see below, even a functional pseudogene constitutes powerful evidence for common descent, if it can be shown that its function is a derived one.

4. Obscuring the issue by appealing to possible functions of pseudogenes

Left: Brain of human embryo at 4.5 weeks, showing interior of forebrain.
Middle: Brain interior at 5 weeks.
Right: Brain viewed at midline at 3 months. Images courtesy of Wikipedia.

In his article over at Answers in Genesis, Dr. Tomkins marshals what he considers to be a strong case that the alleged vitellogenin pseudogene remnant in human beings is actually a functional enhancer element in a gene which is expressed in the human brain:

…[T]he real story is that the alleged 150 base vtg sequence is not a pseudogene remnant at all, but a functional enhancer element in the fifth intron of a “genomic address messenger” (GAM) gene. This particular GAM gene produces long noncoding RNAs that have been experimentally shown to selectively inhibit the translation of known target genes, a majority of which have been implicated in a variety of human diseases. Messenger RNAs from this particular gene are also known to be expressed in a variety of human brain tissues in both fetal and mature subjects in three separate studies. (Bolding mine – VJT.)

Now, I’m no biologist, but I feel bound to point out that two highly respected biologists who are both Christians have highlighted problems with Dr. Tomkins’ arguments.

(a) Venema on why functionality in a pseudogene doesn’t weaken the case for common descent

In part four of his five-part article, which is titled, Vitellogenin and Common Ancestry: Tomkins’ false dichotomy,
Professor Venema explains why functionality in a pseudogene does not invalidate the case for common descent. When scientists study a pseudogene, the question they need to ask is not whether it is functional or not, but whether the functionality is original or derived:

Part of evolutionary theory is the expectation that occasionally some sequences, after losing their original function, may come under natural selection to be repurposed to another function. The technical term for this process is exaptation, and many examples of it are known. Certainly a long, non-coding RNA gene could arise at this location in the human genome and this sequence could be exapted as a regulatory sequence – but there is no hint of admitting this possibility in Tomkins’ work… Rather, it seems enough to Tomkins to suggest that the sequence is functional – and that this alone will be enough for him to convince his readership that this fragment is “not a real pseudogene.”

Put more simply, evidence of function does not erase the evidence for prior history.

Even though the evidence that this sequence is functional in humans is rather thin, the main issue is that even if its function were convincingly demonstrated in the future, it would not remove the evidence that this sequence was once part of a functional VIT gene – evidence that Tomkins has either not addressed, or denied outright. (Bolding mine – VJT.)

(b) Why Dr. Tomkins’ suggestion can’t explain shared synteny

The Evolution News and Views post in response to Professor Venema, titled, Functional Pseuodogenes and Common Descent (May 23, 2016), argues that the vitellogenin pseudogene in human DNA has a function, after all:

Tomkins has presented evidence that the VIT1 pseudogene sits in part of an intron that is transcribed and produces long non-coding RNAs of the type we know often have function.

In her article, The Vitellogenin Pseudogene Story: Unequally Yoked (Evolution News and Views, May 24, 2016), Dr. Ann Gauger goes even further: she addresses the problem of shared synteny (which was discussed above) by proposing that “[t]his similar order could be due either to ancestry or functional reasons.

However, in a recent post on Sandwalk, Professor Larry Moran writes: “There are thousands of lincRNAs but currently there are only about 200 that have known functions and not all of these are even human.” The point Moran makes is a vital one: Function in lncRNA is the exception rather than the rule. As such, the onus is on Intelligent Design proponents to demonstrate a function, rather than merely hypothesizing it.

Four problems with Dr. Tomkins’ proposal

When I contacted Professor Swamidass regarding the argument for the functionality of the long non-coding RNA produced by the VIT1 pseudogene, which was put forward in a 2015 article by Dr. Jeffrey Tomkins and recently defended in several posts over at Evolution News and Views, he had four major criticisms to make regarding the claim that lncRNA has a function, and that it can therefore be explained equally well by the hypothesis of common design.

(i) How important is the function, anyway?

First, it simply isn’t enough to show that the lncRNA is functional in some way. What needs to be shown is that the lncRNA is functional in an important way. Neither Dr. Gauger’s article, nor the article she cites by Dr. Jeffrey Tomkins, demonstrates that the pseudogene has an important function. The vast majority of lncRNAs are not important; they merely express noise. Drs. Gauger and Tomkins make a case that the lncRNA produced by the vitellogenin pseudogene could be important. That doesn’t mean it is important. Just because a lncRNA gets transcribed, it doesn’t necessarily mean that it’s important.

At this point, readers might want to ask: what would constitute reasonable evidence that the lncRNA in question has an important function? That’s a fair question. Professor Swamidass suggested that the discovery of SNPs (single nucleotide polymorphisms) associated with disease in this lncRNA would be good evidence that it is indeed important. While he acknowledged that evidence of this sort might turn up some day, he thought it extremely unlikely.

For the time being, the claim that common design minus common descent is just as good at explaining the genetic evidence explains unsubstantiated.

(ii) The functionality of lncRNA doesn’t depend on its location

The second point made by Professor Swamidass is that Drs. Gauger and Tomkins also need to demonstrate that the functionality exhibited by the lncRNA depends tightly on its being located at this particular position in the genome. The problem here is that in the rare cases when a lncRNA is functional, its functionality is NOT dependent on its position in the genome (it is a trans-acting element, not a cis element). Hence even if the lncRNA in question were functional, Drs. Gauger and Tomkins would still need to explain why it is found in the exact same place in the genome, in mammals and birds. From a design point of view (in the absence of common descent), there would be no reason for this positioning in the genome. To suggest, as Dr. Gauger does in her article, The Vitellogenin Pseudogene Story: Unequally Yoked, that “This similar order could be due either to ancestry or functional reasons” is to engage in unproven speculation about how lncRNAs work, which runs counter to how biologists currently understand their action.

(iii) Position, position, position

Third, Swamidass notes that the explanation proposed by Dr. Tomkins merely attempts to explain the similarity between individual elements (homology), while ignoring their positioning in the genome (synteny). Swamidass considers Dr. Tomkins’ point about homology to be quite reasonable, but it leaves the argument from synteny untouched. Why are the homologous elements positioned in the same way in the genome, in humans, opossums and chickens? Dr. Tomkins supplies no reason.

Now, Dr. Tomkins might wish to argue that in some cases, positioning is important. However, Professor Swamidass informs me that such cases constitute the exception, rather than the rule, in mammalian systems (microbes are a very different matter). The burden of proof is therefore on Dr. Tomkins to show that the order of elements in the human genome is important for the function he proposes.

(iv) The design enigma

Finally, Swamidass raises an interesting theological/philosophical question. Suppose that the vitellogenin pseudogene in humans, and the genes located near it, were all designed. Did the Designer have the power to put these genes in a different order? As far as biologists can tell, this would have been a very easy thing to accomplish. If they are right, then we are confronted with a design enigma: why were we designed in a way which looks just like the pattern we’d expect, if we arose by a process of common descent? (This is especially true for shared synteny, for which we have no biological explanation for except common descent.)

Summing up: the Evolution News and Views articles written in response to Professor Venema endeavor to show that the genetic data relating to pseudogenes is consistent with their having been designed. But the real question is: what is the best explanation of the data? The authors of the ENV articles have not put forward a coherent explanation for shared synteny. For instance, why, if lncRNA is trans-acting, is it located in this place in the genome, AND why is it similar to the VTG gene? The authors do not say.

5. Engaging in wild speculation which goes far beyond the available evidence

The articles attacking Dr. Venema over at Evolution News and Views also rely heavily on speculation which goes far beyond the available evidence, as the following extracts reveal.

The author of the anonymous article, Functional Pseuodogenes and Common Descent (May 23, 2016), proposes that the vitellogenin fragments in humans may turn out to serve some common function
in chickens and humans, in addition to their function of making egg yolk in chickens. Note the speculative language, which I’ve highlighted in bold:

At best, the human vitellogenin “pseudogene” only represents a small fraction of the chicken version of the gene. One could initially surmise that the fragment (or fragments) of the vitellogenin “pseudogene” that humans have (and use for some function) may not be the part (or parts) crucial only for making egg yolk in chickens. We may be using it for a non-egg-yolk related function that’s also found in chickens.

…[Or] perhaps the chicken vitellogenin gene produces not only egg yolk-related proteins, but also RNAs that have other roles or functional interactions in chickens. We may be using our “vitellogenin pseudogene” for a similar RNA-based function or interaction that chickens do…

In either case, our “vitellogenin pseudogene” and the chicken version would turn into a mere example of homologous DNA performing a homologous functions — something we see all the time in biology and which can be explained by common design just as easily as by common descent. It doesn’t appear that the specific function of our “vitellogenin gene” has been explored yet, and this would be an interesting question to investigate. The hypotheses offered here could very well turn out to be true.

In a similar fashion, Dr. Ann Gauger resorts to speculation in her article, The Vitellogenin Pseudogene Story: Unequally Yoked (Evolution News and Views, May 24, 2016), where she argues that even if humans turn out to possess a vitellogenin pseudogene, it appears to have a function which is related to an overlapping gene:

So what if the similarity is statistically significant? What apparent similarity there is could well be due to an overlapping gene with an entirely different function that is present in that stretch of sequence in the chicken, marsupial, dog, and human genomes. (I am guessing it is present in the other genomes — I know it is present in humans.) Indeed, there is evidence of another gene with other possible functions in that region of the genome…

The long non-coding RNAs mentioned above [by Tomkins in his 2015 paper – VJT] are widely believed to have many important regulatory functions in the cell. They are implicated in long- and short-range interactions between genes, the way the DNA loops, whether genes are sequestered or not — all these things and more are affected. (Bolding mine – VJT.)

Two points need to be made here. First, Intelligent Design proponents are fond of holding evolutionists up to ridicule for their speculative proposals on how life may have arisen from inanimate matter, or how macroevolutionary transitions may take place, even in the absence of intelligent guidance. I know; I’ve engaged in this sort of ridicule myself. But we need to be consistent here, or we risk being labeled as hypocrites. If it’s unscientific of evolutionists to engage in speculation about the origin of life or the mechanism of macroevolution in the absence of hard evidence, then it’s equally unscientific of Intelligent Design advocates to engage in speculation about possible functions of gene fragments in the absence of hard evidence. What’s sauce for the goose is sauce for the gander.

Second, the above proposals fail to address the main evidence for common descent cited by Dr. Venema, namely, “the overall match of sequences between placental / marsupial mammals and egg-laying organisms over large spans of DNA, including flanking regions.” It’s the spatial pattern which needs to be explained, and not just the presence of the genes.

6. Use of flawed analogies

In addition to the problems listed above, the Evolution News and Views article, Functional Pseuodogenes and Common Descent (May 23, 2016), makes use of a flawed analogy in its attempt to weaken the case for common descent:

…[A]s a second point, even if humans are using our “vitellogenin gene” for entirely different purposes than chickens do, this still doesn’t provide evidence for common ancestry. Why? Because we often see in technological designs that similar parts can be used for very different purposes. A plastic ring in one design might be used for blowing bubbles, but in another it helps seal the connections between two pipes. Or a plastic container in an outboard boat motor holds fuel, but in another technological design it holds dishwashing liquid. Using similar parts for different purposes is easily accommodated by common design.

I would respond that while a ring can be used for different purposes, we would not expect to find a ring showing signs of wear and tear in a new contraption. The wear and tear suggests that the ring was borrowed from somewhere else. Likewise, the peculiar matching patterns between our vitellogenin pseudogene and those of chickens and opossums, suggests that we are dealing with a gene that has a long history, and that was formerly used for something else. Only common descent can account for the shared synteny described in Professor Venema’s five-part series.

7. Theologizing the argument for common descent

Finally, one of the Evolution News and Views articles responding to Professor Venema makes the mistake of claiming that the case for common descent rests upon theological assumptions. Here’s an excerpt from the anonymous article, Functional Pseuodogenes and Common Descent (Evolution News and Views, May 23, 2016):

The main issue is that evolutionists have commonly argued that non-functionality in shared pseudogenes is what provides evidence for common ancestry. They argue that God would not put “broken” shared DNA in multiple species and thus this must be evidence for common ancestry over intelligent design (or special creation, or whatever). We’ve seen many theistic and atheistic evolutionists treat pseudogenes in precisely this manner…

Evolutionists claim that these pseudogenes provide special evidence for evolution because God would not create different species with shared non-functional DNA in the same location. Therefore, they argue, pseudogenes must be evidence for shared ancestry. (Bolding mine – VJT.)

Let’s be perfectly clear: the argument for common descent can be formulated without resorting to speculation about what God would or would not have done. In order to illustrate this point, imagine that living things on Earth were actually designed by an alien from Alpha Centauri (pictured above), named Alec. If we knew to be the case, what could we infer about the way in which Alec the alien made living things? Quite a lot.

The question of why Alec produced different groups of living things with the same spatial patterns in their genes (shared synteny) would still be a valid one. How might we explain that fact?

We might suppose that Alec kept the original design of the genes on his computer, and then copied it over to the ancestors of reptiles, birds and mammals, on separate occasions. That would be a case of common design without common descent – although it would still invite the obvious question: why would Alec re-use a pattern of genes that served a purpose in reptiles and birds when designing mammals, even though it serves absolutely no purpose in mammals? But the real reason why this explanation is a poor one is that it’s ad hoc: Alec keeps re-using the original design because he feels like it, or he’s too lazy to change it. A much better explanation would be to suppose that from the outset, Alec planned to generate every kind of living thing by a process of common descent from an original stock, intervening only when natural processes were unable to overcome some macroevolutionary hurdle required to generate a new structural design in a class of creatures. Once we impute this original decision to Alec, the rationale for the non-functional similarities in the patterns of the genes of different classes of organisms becomes immediately apparent. What’s more, all of the non-functional similarities can be explained in one fell swoop.

Someone might object that this explanation is ad hoc, too: after all, we might ask why Alec chose to use an evolutionary mechanism to generate the diversity of living things, when he had so many other alternative mechanisms at his disposal. What the objection overlooks is that the best scientific explanations, other things being equal, are the most parsimonious ones. It’s far simpler for scientists to make a single ad hoc assumption than to make a multitude of such assumptions. Consequently, if it were ever proved that life on Earth had been designed by aliens, scientists would still be justified in inferring that they used an evolutionary mechanism to generate the variety of species we see on Earth today.

The above argument assumed that the Designer was an alien, but it would work equally well if the Designer were an angel, or God, or any intelligent agent.

Conclusion

I’d like to conclude with a quote from the young-earth creationist biologist, Todd Wood, whom no-one can accuse of bias:

While common design could be a reasonable first step to explain similarity of functional genes, it is difficult to explain why pseudogenes with the exact same substitutions or deletions would be shared between species that did not share a common ancestor.
(The Chimpanzee Genome and the Problem of Biological Similarity , Occasional Papers of the BSG, No. 7, 20 February 2006, pp. 1-18.)

Why, indeed?

Now, I can certainly understand why someone might feel that notwithstanding the strong scientific evidence pointing to common ancestry, the authority of Scriptural passages which (on a plain reading) teach the special creation of man, such as Genesis 1:26-27, Genesis 2:7 and Genesis 2:21-24, trumps the verdict of science. Fair enough. That’s an argument I can respect. But to deny the strength of the scientific evidence for common descent in the first place is a sign of a peculiar kind of intellectual obstinacy, to my way of thinking.

An overwhelmingly strong scientific case can be made that life on Earth was designed. That alone should be enough to make belief in Intelligent Design reasonable. I believe that we in the ID movement should stick to our strengths. It does our cause no good if we query the very strong scientific evidence for common descent, which in no way weakens the case for Intelligent Design.

303 Replies to “Consider the opossum: the evidence for common descent

  1. 1
    gpuccio says:

    VJ:

    Thank you for insisting on this important point.

    Frankly, I am amazed at the obstinacy with which many people in the ID field stick to denial of the evidence for common descent. I can only think that religious reasons are the cause for that, and certainly that does not speak well for their scientific attitude.

    Biological ID is an amazing and overwhelming scientific theory, the best we have to explain what we observe. Our only hope to defend it against the anti-religious dogma of neo darwinism is to keep a scientifically sound attitude, as unbiased as it is possible for us humans.

    Sticking to views which are as dogmatic as those of our darwinist interlocutors does not help.

    I will say it once again, and I challenge anyone here to prove me wrong:

    The simple observation of the frequency of synonymous mutations in different species is the strongest argument for common descent that we can imagine. I can’t really think of any possible alternative explanation for that simple and universal fact.

    All the rest (pseudogenes, order of genes, and so on) is a bunch of strong arguments too. But the simple evaluation of the rate of synonymous mutations should vastly suffice.

    To be clear, and to avoid the usual misunderstandings, what I am discussing here is descent with designed modifications, and nothing else. We all agree that all the new complex information which arises in all species is designed, and cannot be explained by any neo-darwinian theory, or more generally by any non design theory which does not imply the explicit intervention, in time and space, of some conscious, intelligent and purposeful being as a designer. Not even a single new complex protein can be explained without a designer.

    But descent is all another issue. We cannot deny descent by any reasonable scientific approach. We can accept it with reservations (all scientific theories should be accepted with reservations), we can debate whether descent is universal or not, we can discuss all the inconsistencies of present models of common descent (which, being based largely on neo-darwinian ideas, are probably wrong on many points). But the simple idea of descent cannot be reasonably denied, at least not with what we know at present.

  2. 2
    PaV says:

    vjt:

    You fail to distinguish between “common descent” and “common ancestry.” IOW, Darwinian theory is a theory of gradual change; whereas, ID is a theory of “jumps.” The “jumps” can be so significant that “common descent” becomes a misnomer.

    When there are saltational “jumps,” then we don’t know what goes ‘in-between.’ Personally, I don’t think this ‘gap’ will ever be closed. I don’t see how it can be.

    In the absence of this ‘gap’ being closed, we cannot definitely affirm “common descent.”

  3. 3
    bill cole says:

    VJT thanks again for surfacing this important debate.
    Gpuccio

    But descent is all another issue. We cannot deny descent by any reasonable scientific approach. We can accept it with reservations (all scientific theories should be accepted with reservations), we can debate whether descent is universal or not, we can discuss all the inconsistencies of present models of common descent (which, being based largely on neo-darwinian ideas, are probably wrong on many points). But the simple idea of descent cannot be reasonably denied, at least not with what we know at present.

    I think the idea of common decent may be completely wrong and should be examined carefully. The alternative is that we are facing billions of origin events that are not connected except by common biochemistry . I think we understand less than 1% of a eukaryotic cell at this point so the arguments for common decent are arguments from ignorance. Are these really pseudo genes or do they have function we do not understand? In all due respect I think that the sequential space of the genome, which I know you understand very well, makes this common decent story iffy at best. Can we mathematically model a single transition? I think it is time to get this fairy tale of a theory off the drugs and into reality. Decent with design modification is supposing we have a clue how diversity unfolded. Do we really? Have we looked at the differences in splicing codes and gene expression timing. VJT is looking at the similarities. How about the differences? Is the origin of man an event that we can biochemically reconcile?

  4. 4
    mw says:

    Thank you vjt for another skillfully written article.

    —————————
    “Now, I can certainly understand why someone might feel that notwithstanding the strong scientific evidence pointing to common ancestry, the authority of Scriptural passages which (on a plain reading) teach the special creation of man, such as Genesis 1:26-27, Genesis 2:7 and Genesis 2:21-24, trumps the verdict of science. Fair enough. That’s an argument I can respect. But to deny the strength of the scientific evidence for common descent in the first place is a sign of a peculiar kind of intellectual obstinacy, to my way of thinking.”
    —————————-
    Therefore, at Sinai, the Holy Trinity through Yahweh, was obstinate enough to claim God created in six days to a gullible Moses?

    Judaeo-Christians should  start the origin debate at historic Sinai, then we may look back more confidently to Genesis, and forward to the Transfiguration.

    Are we to say, Jesus at the Transfiguration, spoke to an obstinate lawgiver, given by an obstinate God/Jesus Himself?

    However, strength of consensus science, is not the same as stating, common descent is a scientific law, for that would be a ‘whopper.’

    As for the strength of ID; in my opinion, it rests on the objective observation, that pattern exists, with design,  irreducible in complexity, and interrelated  to other equally irreducible complex system in life units, life forms and life components.

    The courageous step is, such intelligence was above human capabilities, and above what Darwinism has come to be.

    In the case of Darwinism, no divinity is allowed. In the case of ID, divinity is allowed. Of course, there is theistic evolutionism and theistic ID evolutionism, so it appears to me in this case.

    It seems one of the strengths of ID, is that many interpretations at uncommondescent appear to be tolerated, just about.

    To impose one singular belief into ID, when later, other science may prove more beneficial to a differing view, would be detrimental to the movement at present.

    Be that as it may: to return to the topic. In relation to Genesis, and the special creation of humans, you say you can “respect” that.

    Surely vjt, you also respect divine clear law, the fulfillment of Genesis, as law, given with power, and as an historic stone written document, carried with upmost honour, surrounded by miracle after miracle for forty years.

  5. 5
    mk says:

    hi vj.

    i dont think that the pseudo vit genes are evidence for a commondescent for 2 reasons:

    1)the vit protein is a multifunctional. so even if it was active in humans it can function for other function then making yolk.

    2)the fact that all those inactivation can happan convergently in many species (tooth loss for example happaned convergently about 10 times in 10 different species).

    therefore a pseudo vit cant be consider as an evidence for a commondescent.

  6. 6
    mike1962 says:

    VJT: +1

    Gpuccio: +1

  7. 7

    VJ, thanks for another excellent post.

    This has been a fascinating debate to follow, and I respect the ID community for working so hard to grapple with the genetic evidence here. An honest appraisal of the evidence here really goes a long way in building trust with those outside your community.

    I might comment on specific science points later (not sure), but I did want to expand on a few points:

    Glen Williamson’s contribution is very significant here:

    “About 1,500 base pairs can be aligned with around 73% identity. That’s much more than the 150 base pairs that Tomkins chose to focus on. Readers will recall that Tomkins claimed only a 62% identity, even for this short segment.”

    If you look at the e-values, they are very very low, indicating that the match is very certain. Of course, critics can parse Venema’s argument (e.g. what is the exact definition of a pseudogene, was that 150bp the right place to focus), but his argument is based on this DNA sequence match. This match is, unequivocally, statistically very very strong. Of course, comparatively, the possum match is stronger still (which is consistent with a later loss). This is exactly what we expect from CD.

    I will also comment on this point:

    “At this point, readers might want to ask: what would constitute reasonable evidence that the lncRNA in question has an important function? That’s a fair question. Professor Swamidass suggested that the discovery of SNPs (single nucleotide polymorphisms) associated with disease in this lncRNA would be good evidence that it is indeed important. ”

    A SNP-disease association would be helpful but not definitive (sometimes SNPs are markers for nearby disease genes). More precisely, evidence that a mutation here causes some disease or phenotype would be helpful. There is a large body of literature that shows the hard science needed to make this case. The problem, though, is that the vast majority of mutations and SNPs in noncoding regions (like lncRNAs) are totally inconsequential.

    Another strategy would be to take human cells and use a technology like CRISPR to delete this lncRNA, and see if this changed the cell’s behavior in any way. Gene expression would be a good starting point, but ultimately we would have to see a strong connection to phenotype to be convinced that this specific lncRNA was important.

    To be clear, I’m just explaining the current standards for making the biological argument that this lncRNA is truly is functional in any meaningful sense of the word. Short of this, the claim that this is “functional” is just speculation, unsubstantiated hypothesizing. More importantly, given what we know of biology, it is likely to be an incorrect hypothesis. lncRNAs are not usually important.

    Moreover, @5 this lncRNA does NOT even cover the entire similar region. Even if, against all odds, this lncRNA really is functional (when most are not), this does not explain the why the rest of the region is similar. And, to be clear, VTG is NOT active in humans; no evidence suggests it is translated into functional protein. Rather, VTG is a pseudogene. At the same time, one small piece of VTG1 might (with very low probability) also be an example exaptation to form a new functionally important lncRNA. This, however, is purely speculation, because lncRNAs are usually not functionally important (only rarely they are).

    Also @5, look at the original article. It explains eloquently why expect convergent loss of VTG genes in different mamalian lineages: http://journals.plos.org/plosb.....io.0060063

    Once again, enjoying the debate. Looking forward to see how it progresses.

  8. 8
    Dr JDD says:

    Really, lncRNA’s are mostly non-functional and rarely functionally important?

    How comes a quick pub med search of “lncRNA cancer” yields over 2000 published hits? How comes these regulatory RNAs (along with a raft of others) is receiving such attention in the field of oncology and actively pursued by pharma and biotech companies alike?

    http://www.ncbi.nlm.nih.gov/pubmed/27233618

  9. 9
    Origenes says:

    VJTorley seems to misinterpret what Ann Gauger is saying.

    VJTorley quotes Ann Gauger:

    Patches of sequence similarity to the chicken genome that might be interpreted as pseudogenes can be found in syntenic regions of marsupial genomes.

    [emphasis VJTorley]

    And VJT goes on saying:

    Dr. Gauger minimizes the significance of the evidence for vitellogenin pseudogenes VIT2 and VIT3 in marsupials (such as opossums) by saying that it “might be interpreted as pseudogenes.” In other words, she’s not even sure that opossums possess these pseudogenes.

    No, that’s not what she is saying. Here Ann Gauger expresses her doubts about the aptness of the term “pseudogenes” wrt vitellogenin genes VIT2 and VIT3. Ann Gauger has doubts about the soundness of the evolutionistic concept of pseudogenes. Notice also her use of quotation marks, earlier in her article, when she wrote:

    These “inactivated” genes are called pseudogenes, and are taken by evolutionists as further evidence for common descent.

  10. 10
    bill cole says:

    VJT

    Swamidass comments that by citing this passage from Dr. Tomkins, which defines pseudo-genes in terms of their total lack of functionality, Dr. Gauger has effectively changed the definition of a pseudogene, setting aside the standard definition. Even if VTG in humans were a lncRNA with an important function, it would still be a pseudogene, because no protein is being expressed from it and it exhibits similarity to VTG in chickens, and is in the correct place in the genome.

    This statement is a big stretch with many assumptions. We don’t know any mechanism that can take a gene and transform it into a lncRNA. The statement is therefor circular because you are assuming this lncRNA came from a gene just because of sequence homology. Again, this is highly unlikely with RMNS neutral theory or any other known evolutionary mechanism.

  11. 11
    bill cole says:

    VJT

    Finally, Swamidass raises an interesting theological/philosophical question. Suppose that the vitellogenin pseudogene in humans, and the genes located near it, were all designed. Did the Designer have the power to put these genes in a different order? As far as biologists can tell, this would have been a very easy thing to accomplish. If they are right, then we are confronted with a design enigma: why were we designed in a way which looks just like the pattern we’d expect, if we arose by a process of common descent? (This is especially true for shared synteny, for which we have no biological explanation for except common descent.)

    Do you really think the last sentence here is credible? No biological explanation other than common decent? The designer made the genome a sequence the same mathematical space as our language. Alternative splicing is an extension of this design. IMHO he did not need to do anything else to show that new species required new designed sequences. Can you name any known mechanism that can generate a sequence other than intelligence? The fact that FUNCTIONAL SEQUENCES changed as much at they have is a show stopper for common decent by any known evolutionary mechanism.

  12. 12

    @8 lncRNAs are only rarely important. This paper is a good overview (no paywall): http://www.ncbi.nlm.nih.gov/pm.....MC4306305/

    “Although the estimated number of different types of human lncRNAs has ranged from 5,400 to 53,000 (Table ?Table22), only a small fraction have been found to be present at levels high enough to suggest that they have a function. According to ENCODE’s own estimates, fewer than 1,000 lncRNAs are present at greater than one copy per cell in the typical human tissue culture cell line (Djebali et al., 2012; Palazzo and Gregory, 2014), although some other estimates have determined that the levels may be substantially higher (Hangauer et al., 2013)”

    To be clear, of the 1,000 lncRNAs that are expressed above 1 copy per cell (<2% of lncRNAs), very few have been demonstrated to be functional. Moreover, lncRNAs are very easy to generate by mutation, so even those that are functional in cancer may very well be de novo lncRNAs that are not part of the normal function of normal human cells.

    The whole article is worth reading for those curious about the science behind this.

    @10 Bill says, "We don’t know any mechanism that can take a gene and transform it into a lncRNA."

    lncRNA = long non-coding RNA
    RNA = transcribed; non-coding = not translated

    This means any part of the genome that is transcribed more than 100 bases but not translated is a lncRNA.

    We do know a mechanism for making lncRNA from functional genes. Take a functional gene, that produces protein. Mutate it enough to break it, so that it no longer can produce a protein, but not so broken that it is no longer transcribed. There, are of course, many ways to do this (1) adding a stop codon, (2) mutate out the shine delgarno sequence https://en.wikipedia.org/wiki/Shine-Dalgarno_sequence, (3) remove the initating ATG, or (4) add an early indel. This all happens naturally if you mutate a gene. Of course, transcription uses totally different signals (like the TATA box), so it is easy to imagine (and experimentally verify) mutants that transcribe non translated RNA after a gene breaks.

    So, genes that break often become lncRNAs. We have a clear mechanism for producing non-functional lncRNAs from functional genes. I hope no one disputes this.

    This is a key point, lncRNAs are usually broken coding genes, i.e. they are usually pseudogenes. Functional lncRNAs are the exception, not the rule.

    The VTG lncRNA under question appears to be an inactivated functional gene. Moreover, lncRNAs do not produce protein, therefore it is a pseudogene even if it is found to have another regulatory function. Even if it now (by exaptation) has an important function in gene regulation (speculative and very unlikely), its function is trans-acting. Therefore, there is no functional reason for it to be at this position in the genome. The sytentic evidence for CD here remains strong.

    All this is beside the point. The VTG lncRNA under question appears to be an inactivated functional gene, and a small portion of it is now a non-functional lncRNA. It is a pseudogene.

  13. 13
    bill cole says:

    Hi Dr Swamidass

    We do know a mechanism for making lncRNA from functional genes. Take a functional gene, that produces protein. Mutate it enough to break it, so that it no longer can produce a protein, but not so broken that it is no longer transcribed. There, are of course, many ways to do this (1) adding a stop codon, (2) mutate out the shine delgarno sequence https://en.wikipedia.org/wiki/Shine-Dalgarno_sequence, (3) remove the initating ATG, or (4) add an early indel. This all happens naturally if you mutate a gene. Of course, transcription uses totally different signals (like the TATA box), so it is easy to imagine (and experimentally verify) mutants that transcribe non translated RNA after a gene breaks.

    You are describing a very long journey through essentially infinite sequential space and you are describing a process not a mechanism. If you can model this mathematically showing a functional lncRNA from a gene derived from a identified mechanism I will buy you dinner anywhere you like in the LA area in July:-)

  14. 14
    ThickPython says:

    Hi Dr Swamidass,

    I ran that blast literally as I was getting the kids ready for school so it’s a very quick analysis!

    And as Vincent mentioned, I carved out a small chunk (4Mbp) of the human chromosome 1 so that it would run faster. That point needs to be emphasised because I know you talked about the e-values being very low, but the true e-values are slightly higher because the true search space is larger. I still agree though that the match is virtually certain.

    What you can see from the BLAST results is that the chicken VTG1 gene is about 43kbp, while the results in the human genome span about 75kbp. If ‘one’ had the time (if that ‘one’ is me then I don’t have the time) then one could construct a consensus sequence for the gene both in the mammalian and avian lineages, and I imagine that would result in much greater synteny.

    As much as I would love to rub that in Dr Tomkins face, I just don’t have the time at the moment.

  15. 15
    PaV says:

    Where did the first bird feather come from?

  16. 16
    Mung says:

    Where did the first bird feather come from?

    It came from a bird.

  17. 17
    Mung says:

    I too wonder at the objections to common descent. But then, I also wonder why people thought Jesus was going to return in 1987.

    Even the most ardent young earth creationist accepts common descent. So, where’s the beef?

    To the young earth creationists here at UD:

    Pick a group of modern species that you believe is related by common descent. Their ancestors came off the ark along with Noah and his family. They multiplied and diverged.

    What evidence and/or arguments would you offer in favor of your theory of common descent that would be accepted by someone who thinks each species was individually seeded on earth by aliens last Thursday?

  18. 18
    Mung says:

    In a nutshell, Professor Venema’s argument is that shared synteny is best explained by the hypothesis of common ancestry.

    Awesome. And we know it’s the same chromosome because they share the same genes! Therefore common descent. I’m probably wrong.

    How do we know that a given chromosome is shared by two species due to common descent? How do we answer this question without begging the question?

  19. 19

    @14 ThickPython thanks for your work in this. I think you added a lot.

    A couple thoughts…

    1. This is a minor point (because it does not change the interpretation), but because we are a priori only looking in the region near ELTD1, the e-values do not need to be adjusted for the whole genome. Of course, even if we do, this is still a clear match. This is notable because BLAST is not even designed to pick up remote homologies like this. The original authors used SIM, a different algorithm designed specifically for this task. Regardless, the match is absolutely statistically significant.

    2. Reader can check this themselves with this recipe:

    a) Get the VTG1 sequence from here:
    http://www.ncbi.nlm.nih.gov/gene/424547
    http://www.ncbi.nlm.nih.gov/nu.....o=18737086

    b) Paste sequence into blastn website (default parameters, https://blast.ncbi.nlm.nih.gov/Blast.cgi). Choose to search against HUMAN…and you get these three top genomic regions…

    Homo sapiens chromosome 1, alternate assembly CHM1_1.1 291 1.613e+06 9% 5e-74 75% NC_018912.2
    Homo sapiens chromosome 1, GRCh38.p2 Primary Assembly 291 1.288e+06 8% 5e-74 75% NC_000001.11
    Homo sapiens chromosome 15, alternate assembly CHM1_1.1 181 6.026e+05 4% 6e-41 71% NC_018926.2
    To summarize here, about 9% (much larger than 150bp) of vtg1 maps to human non-coding region with 75% identity. The first two matches are duplicates of the same region of Chr 1 (the correct place, different assemblies) with e-values of 5×10^-74. The nearest match after that has an e-value of 6×10^-41. This Chr 15 match is a reasonable negative control. So I would accept a “corrected” e-value of 10^-33 (which is definitely better than 0.05 p-value).

    c) Now, we can also visualize this using the UCSF genome browser BLAT search. Just paste the VTG1 sequence into BLAT (https://genome.ucsc.edu/cgi-bin/hgBlat?command=start). Click the first hit, then zoom out far enough to see ETLD1 and check the tracts as required. I did this to get this image here:

    https://genome.ucsc.edu/cgi-bin/hgTracks?db=hg38&lastVirtModeType=default&lastVirtModeExtraState=&virtModeType=default&virtMode=0&nonVirtPosition=&position=chr1%3A78659897-78919796&hgsid=497817261_89LABjkhtaZ9Vn8cDAIDVganAACJ
    http://swami.wustl.edu/hgt_genome_680f_62a4d0 (if the first one doesn’t work use this).

    A couple things to note. (1) the sequence is right where we expect it to be, (2) in my image, I plotted the match alongside transcript levels. The VTG1 match is not expressed nearly at all (because it is not likely functional) while the two flanking genes (see bar graphs) are expressed in a large number of tissues at a high level.

    To reiterate, Gauger and Tomkins do not even discuss this evidence at all. This is only the VTG1 gene itself. There are even more matches if we include the sequence before and after the VTG1 gene (which I did not do here). None of this is addressed. All they do is make the dubious claim that (1) this match is not significant and (2) it is functional (it is not).

    3. On a related note, have you considered making recipes for these sorts of analysis available on bitbucket or github for people to download themselves and run the analysis? I wonder if that could help bring people along. Another option would be synapse. https://www.synapse.org/. What do you think?

  20. 20
    Robert Byers says:

    We are not mammals. We just have like traits for like needs from a common blueprint.
    Saying common descent is proved from like traits means having eye balls proves a eyeball common ancestor.
    Its all just a comparative paradigm including comparing genetics..
    Common descent is not demonstrated by biological evidence and the articles biting at this on Evolution news are right on.
    lets see some real evidence for common descent and not claims its proved.

  21. 21
    bill cole says:

    Mung

    I too wonder at the objections to common descent. But then, I also wonder why people thought Jesus was going to return in 1987.

    Even the most ardent young earth creationist accepts common descent. So, where’s the beef?

    The beef is that without a mechanism it is bad science. It was paired with RMNS and does not work without it. It proposes that animal a and b split from common ancestor c by natural causes. With RMNS and neutral theory in doubt because the size of the sequential space of the genome it has no natural mechanism to validate it as a concept. Every time I have seen credible evidence to make CD a competing inference like fused chromosome 2 that evidence gets invalidated. This is a real bag of worms. Look at Python identifying almost 2x the genome space in humans vs chickens. How in the world 4^32k of additional sequential genome space functionally organize itself right next to the chicken version. You have to be kidding me 🙂

    How do we know that a given chromosome is shared by two species due to common descent? How do we answer this question without begging the question?

    Exactly
    colewd

  22. 22

    @13 Bill =)…

    To be very clear, I am claiming that this is a NON-functional lncRNA because there >98% of lncRNAs are functional and no evidence has been presented that indicates that this specific lncRNA is functional.

    So the math is easy. (1) start with a functional VTG1 gene. This gene is being transcribed into RNA and then translated into protein. (2) mutate this gene so we BREAK its ability to be translated. There should be no debate here, ID has not problem with the notion that mutations can break things, right.

    Tada!!!! We have a lncRNA, because this RNA is long, and now it is non-coding. It does not have to evolve any more function than this. Losing the ability to code protein makes it a lncRNA. We are done.

    I already explained several ways this could be done. (1) adding a stop codon, (2) adding an indel no divisible by 3, (3) breaking the Shine-Delgarno sequence, (4) mutating out the initiating ATG (yes, just on bp mutation can do it in many cases), OR (5) several other mechanism. The exact math depends on local mutation rate, but really any one of these pathways can break the coding function gene, transforming it into a NON-functioning lncRNA.

    There is no large sequence space to explore. We are just LOSING a function (protein coding), not gaining one.

    So, in my humble opinion, I think I deserve that dinner =). Though, I admit, I didn’t precisely answer your question because it was phrased differently than my initial claim.

  23. 23

    @20 Byers…

    Did you read the article? Why do we (humans) need a broken egg yolk gene in our genomes? What is the reason for this?

    @21 Bill…

    The Chr2 fusion is real. I think you were fed some misinformation. Did you see these posts by ThickPython?

    https://roohif.wordpress.com/2016/05/14/chromosome-2-fusion-the-low-hanging-fruit/
    https://roohif.wordpress.com/2016/05/29/chromosome-2-fusion-dead-in-a-day/

    Notice how some have put our false information about Chr2 fusion out there. If this is important to you, I encourage you to learn how to do the analysis yourself. ThinkPython is a great example to us all here.

  24. 24
    bornagain77 says:

    Although Darwinists and Theistic evolutionists think they have proven their case for common ancestry with sequence comparisons, there are some major problems with some of the assumptions that they are making in their supposed ‘proof’ for common ancestry.

    First off, they apparently erroneously believe that mutations to DNA will tell us something important about how it is possible to transform one kind of creature into another kind of creature. They are wrong in this basic assumption of theirs.

    They, both theistic evolutionists and atheistic Darwinists, simply have no solid scientific evidence whatsoever that it is possible to transform one kind of creature into another kind of creature simply by mutations to DNA alone. In other words, they have made an enormous, and completely erroneous, assumption that DNA sequences tell us something vitally important for the hypothesis of common ancestry when the fact of the matter is that DNA sequences tell us next to nothing about how it is even remotely possible to change one kind of creature into another kind of creature.

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    Dr Stephen Meyer states that you can mutate DNA ’til the cows come home’ and it still won’t help:

    ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body-plan. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’
    Stephen Meyer – Functional Proteins and Information for Body Plans – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1140536289292636/?type=2&theater

    Moreover, these ‘pointless’ sequence comparisons, that atheistic Darwinists and theistic evolutionists put so much faith in, sequence comparisons that are shown to have nothing important to do with establishing whether it is even feasible to transform one kind of creature into another kind of creature, also highlight the unfalsifiable nature of evolutionary thinking.

    In other words, if similar sequences in supposedly closely related species are suppose to be knock down proof of common ancestry, as their reasoning goes, then why in blue blazes does the fact that similar sequences are found in distantly non-related species not then count as falsification to that hypothesis? Cherry picking only the evidence that agrees with your preferred hypothesis whilst completely ignoring evidence that falsifies your hypothesis in certainly not the practice of sound science!

    Research shows that corals share many of the genes in the human genome – June 1, 2016
    Excerpt: UH M?noa scientists,,, have published new research showing that corals share many of the genes humans possess, especially those that can sense temperature and acidity, both of which are important to keeping both coral and humans healthy.,,
    “it was surprising to find that corals share many of the genes we possess,” said Dr. Stokes.
    http://phys.org/news/2016-06-c.....enome.html

    Shark and human proteins “stunningly similar”; shark closer to human than to zebrafish – December 9, 2013
    Excerpt: “We were very surprised to find, that for many categories of proteins, sharks share more similarities with humans than zebrafish,” Stanhope said. “Although sharks and bony fishes are not closely related, they are nonetheless both fish … while mammals have very different anatomies and physiologies.
    http://www.uncommondescent.com.....zebrafish/

    Where could we have learned but from Phys.org – Sept. 28, 2014
    Excerpt: “We have basically the same 20,000 (30,000?) protein-coding genes as a frog, yet our genome is much more complicated, with more layers of gene regulation.”
    http://www.uncommondescent.com.....-phys-org/

    Efforts to make and apply humanized yeast – Oct. 13, 2015
    Excerpt: A large proportion of yeast protein-coding genes that have been tested can be replaced with their human orthologs.
    http://bfg.oxfordjournals.org/.....l.pdf+html

    Kangaroo genes close to humans
    Excerpt: Australia’s kangaroos are genetically similar to humans,,, “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order,” ,,,”We thought they’d be completely scrambled, but they’re not. There is great chunks of the human genome which is sitting right there in the kangaroo genome,”
    http://www.reuters.com/article.....P020081118

    On Human Origins: Is Our Genome Full of Junk DNA? Pt 2. – Richard Sternberg PhD. Evolutionary Biology – podcast
    Excerpt: “And here is another example. They are now sequencing the nuclear DNA of the Atlantic bottle-nose dolphin. And when they started initially sequencing the DNA, the first thing they realized is that basically the Dolphin genome is almost wholly identical to the human genome. That is, there are a few chromosome rearrangements here and there, you line the sequences up and they fit very well. Yet no one would argue, based on a statement like that, that bottle-nose dolphins are closely related to us. Our sister species if you will. No one would presume to do that. So you would have to layer in some other presumption. But here is the point. You will see these statements throughout the literature of how common things are.,,,
    (So when you get to the folder and the super-folder and the higher order level, that’s when you find these striking differences.)
    http://www.discovery.org/multi.....-dna-pt-2/

    I read somewhere earlier where a Theistic evolutionist on this blog claimed that those who reject common ancestry are only doing it for religious reasons. Dr. Hunter would have more than a few words to say to that hypocritical slander!

  25. 25
    HeKS says:

    Prof. Swamidass @23

    The main issue with Chromosome 2 fusion is not whether or not it happens to actually be a fusion, but that even if it is it tells us nothing about evolution or common ancestry, because it was not inherited. It would simply be a fusion that occurred within the human population.

    Take care,
    HeKS

  26. 26
    HeKS says:

    Prof. Swamidass @7

    You said:

    Another strategy would be to take human cells and use a technology like CRISPR to delete this lncRNA, and see if this changed the cell’s behavior in any way.

    Denis Noble (and probably others) has previously addressed the problem with attempting to prove non-function through various kinds of knock-out experiments. The issue is that, in many cases, there are multiple layers of redundancy that are only triggered when primary (and sometimes even secondary and/or tertiary, etc.) functions fail, and perhaps only under specific circumstances. This means that you might knock something out, note that you aren’t seeing any resulting change in the cell (or the organism as a whole, or whatever level of specificity you happen to be considering), and conclude that what you’ve knocked out has no function, when the reality of the matter is that you may not have seen any difference because what you’ve knocked out would typically not be required to be actively doing anything under the current conditions, in spite of the fact that it is a fully functional piece of code. For this reason, knock-out experiments can be useful in definitively establishing function, but under normal circumstances they are not good for definitively establishing non-function.

  27. 27
    Andre says:

    As we have already established common descent is first and foremost an asumption. So I share some genes and some some sequences with a chicken. Could it have been common descent? Sure it can but it is equally valid that it could also be common design.

    But never ever forget you are basing what you think true on an assumption.

  28. 28
    ThickPython says:

    @Bornagain77, #24.

    Please stop Gish-galloping. Nearly all of your comments here at UD are enormously long, and would take an enormous amount of time to dissect. So .. I’ll only look at one: Some shark proteins are closer to humans than they are to zebrafish? And you think that falsifies common descent?

    Let me draw an analogy. What if I told you that some shark proteins are closer to the gray wolf than they are to the coyote – what would you say? “Whoopty-frikkin-doo”, right? They’re basically the same animal, so by sheer luck, the shark will be closer to one of them over the other. This is the same scenario you have with the shark, human and zebrafish: the human and the zebrafish have exactly the same amount of time separating them from the shark. Both the human and the zebrafish have to go back some ~500 million years before they share a common ancestor with the shark.

    I think where you’re going wrong is that you’re mistaking the statement “out of the human and the zebrafish, the shark is closer to the human” for “out of the zebrafish and the shark, the human is closer to the shark”. The first one is basically a coin-flip, while the second would cause some problems for common descent.

    That’s not to say that the results of the study weren’t surprising – they are – but they do not contradict common descent.

  29. 29
    ThickPython says:

    The main issue with Chromosome 2 fusion is not whether or not it happens to actually be a fusion, but that even if it is it tells us nothing about evolution or common ancestry, because it was not inherited. It would simply be a fusion that occurred within the human population.

    100% agree. The fusion in chromosome 2 is NOT evidence for either position. It tells is nothing about common descent.

  30. 30
    ThickPython says:

    @Prof Swamidass:

    On a related note, have you considered making recipes for these sorts of analysis available on bitbucket or github for people to download themselves and run the analysis? I wonder if that could help bring people along.

    Yeah I’ve considered it, but in the end it may be more effort than it’s worth. To do any serious work you probably need your own Linux server and that in itself limits the audience quite a bit. I’m happy to post all my code online .. but, for example, I don’t expect lay people to be able to write Postscript code to draw a diagram of the fusion 🙂

  31. 31
    tommy hall says:

    ThickPython: “Please stop Gish-galloping. Nearly all of your comments here at UD are enormously long, and would take an enormous amount of time to dissect.”

    I’m mostly just a lurker here, but I love and appreciate Bornagain’s posts….he often posts links to things I’ve never seen or read before…stuff I probably wouldn’t come across on my own….lots of good insight….so thanks, BA, and keep up the good the work 🙂

  32. 32
    ThickPython says:

    @tommy, #31:

    “I’m mostly just a lurker here, but I love and appreciate Bornagain’s posts”

    Well Tommy here’s a test. Do you believe that the shark-human-zebrafish article is a problem for common descent?

    Keen for the chromosome 2 hangout whenever you are. You appear to be ignoring my requests …

  33. 33

    @26 HEKS.

    You are correct. Proving this lncRNA function is not easy, especially because there is no obvious evidence that it is functional.

    Unfortunately, the onus is on those that claim this lncRNA is functional to prove it. The current understanding of biology is that 99% of lncRNA’s are non-functional. In fact, 98% are not even expressed at more than 1 copy per cell, as far as we can tell.

    I will say, there might even be a Nobel Prize in it for someone who can demonstrate that most lncRNAs are functional. That would so overturn our current understanding of how biology works that the committee would likely take notice.

    Coming back down to earth, absent any additional evidence this putative lncRNA is most likely non-functional. From a CD perspective, it is most likely a leftover remnant of the previously functional VTG1 gene, or even just “noisy” gene expression and not a lncRNA. Certainly not anything that makes us doubt that that humans have an egg pseudogene in our genomes.

    Once again, if we reject common descent, why do we have this broken gene? What design principle explains this pattern?

    Maybe CD + design is a good possibility, but design alone does not explain this.

    @29

    I disagree. The Chr2 fusion is evidence because (if we agree for a moment on the claim) the fusion looks very much like what we expect from a known chromosomal lesion.

    This data a great deal of sense in CD, given what we know of biology If, on the other hand, humans had Chromosomes that looked totally different, this would entirely end the notion that chimps and humans have a common ancestor. This evidence is entirely consistent with CD, when there is no design reason it needed to be. Of course it is consistent with design too, but why would we be designed to look like we had a modified version of ape chromosomes if not CD?

    Of course, this could have been a designed modification. But CD predicts that all the changes we see will map to biochemical mechanisms we can study. There is no reason for this to be the case, yet is what we see.

    At the very least, we need to acknowledge that disproving CD and evolution does not appear to be part of the Designer’s goals. It would be so easy to invalidate evolution if the Designer has given us different genomes. He did not. Why not? Apparently arguing against CD was not nearly as important to him some might hope.

    @27

    To be clear Andre, this CD is not an assumption. It is an explanatory framework that enables us to accurately predict a large number of patterns we see in genomes (like broken egg yolk genes in humans). CD is a way of generating hypothesis that usually end up being correct, especially when we look at recent evolutionary history (like human evolution).

    CD is not an assumption. Data could easily invalidate it. The evidence, however, supports it. In contrast, it is hard to imagine data that would invalidate design (I’m sure it exists). CD is falsifiable. It just is not falsified by genomes we find in nature.

  34. 34
    ThickPython says:

    @Prof Swamidass, #33:

    The Chr2 fusion is evidence because (if we agree for a moment on the claim) the fusion looks very much like what we expect from a known chromosomal lesion.

    Of course we agree on the claim, there’s no doubt that it is a fusion. But it happened in the human lineage only – there are no evolutionary relationship revealed by it.

    Hypothetically at least, it is consistent with the creationist view that humans and chimpanzees were created separately … and then the fusion occurred in the human lineage.

  35. 35
    Andre says:

    Thickpython.

    Well Tommy here’s a test. Do you believe that the shark-human-zebrafish article is a problem for common descent?

    When we assume something, nothing can be a surprise, heck there are people out there that believe mud became alive all by itself…..

    You do know that common descent is just an assumption right?

  36. 36
    Andre says:

    Thickpython

    Please stop Gish-galloping. Nearly all of your comments here at UD are enormously long, and would take an enormous amount of time to dissect. So .. I’ll only look at one: Some shark proteins are closer to humans than they are to zebrafish? And you think that falsifies common descent?

    If you are unable to cordially allow differing opinions on an assumption can I request that you rather not post here? Keep it civil and stop throwing insults at people that disagree with you.

  37. 37
    Andre says:

    I will help everyone with the meaning of the word assumption.

    as¦sump|tion

    NOUN

    1.a thing that is accepted as true or as certain to happen, without proof

  38. 38
    bornagain77 says:

    as to

    “And you think that falsifies common descent”

    and

    “CD is not an assumption. Data could easily invalidate it. The evidence, however, supports it. In contrast, it is hard to imagine data that would invalidate design (I’m sure it exists). CD is falsifiable. It just is not falsified by genomes we find in nature.”

    Contrary to what you ‘religious’ guys falsely believe, nothing is ever allowed to falsify Darwinian evolution, at least nothing that Darwinists will ever accept.

    “Being an evolutionist means there is no bad news. If new species appear abruptly in the fossil record, that just means evolution operates in spurts. If species then persist for eons with little modification, that just means evolution takes long breaks. If clever mechanisms are discovered in biology, that just means evolution is smarter than we imagined. If strikingly similar designs are found in distant species, that just means evolution repeats itself. If significant differences are found in allied species, that just means evolution sometimes introduces new designs rapidly. If no likely mechanism can be found for the large-scale change evolution requires, that just means evolution is mysterious. If adaptation responds to environmental signals, that just means evolution has more foresight than was thought. If major predictions of evolution are found to be false, that just means evolution is more complex than we thought.”
    ~ Cornelius Hunter

    What the vast majority of Darwinists, and Theistic evolutionists, fail to realize (or to ever honestly admit to) is that Darwinian evolution is not even a ‘real’ physical science in any proper sense that can be tested, but that Darwinian evolution is more realistically thought of as a pseudo-science. Even Jerry Coyne himself, the self-appointed Grand Inquisitor of Darwinian evolution, who won the ‘censor of the year award’ in 2014 from ENV, admits that Darwinian evolution lacks all the rigor one expects of a proper physical science:

    “In science’s pecking order, evolutionary biology lurks somewhere near the bottom, far closer to phrenology than to physics. For evolutionary biology is a historical science, laden with history’s inevitable imponderables. We evolutionary biologists cannot generate a Cretaceous Park to observe exactly what killed the dinosaurs; and, unlike “harder” scientists, we usually cannot resolve issues with a simple experiment, such as adding tube A to tube B and noting the color of the mixture.”
    – Jerry A. Coyne – Of Vice and Men, The New Republic April 3, 2000 p.27 – professor of Darwinian evolution at the University of Chicago

    And without any way to test, and potentially falsify, Darwinian evolution in the real world, it simply fails to qualify as a real science.

    “In so far as a scientific statement speaks about reality, it must be falsifiable; and in so far as it is not falsifiable, it does not speak about reality.”
    Karl Popper – The Two Fundamental Problems of the Theory of Knowledge (2014 edition), Routledge

    “Darwinism is not a testable scientific theory, but a metaphysical research program.”
    Karl Popper – Unended Quest: An Intellectual Autobiography (1976)

    Dubitable Darwin? Why Some Smart, Nonreligious People Doubt the Theory of Evolution By John Horgan on July 6, 2010
    Excerpt: Early in his career, the philosopher Karl Popper ,, called evolution via natural selection “almost a tautology” and “not a testable scientific theory but a metaphysical research program.” Attacked for these criticisms, Popper took them back (in approx 1978). But when I interviewed him in 1992, he blurted out that he still found Darwin’s theory dissatisfying. “One ought to look for alternatives!” Popper exclaimed, banging his kitchen table.
    http://blogs.scientificamerica.....evolution/

    The primary reason why Darwinian evolution cannot be tested in the real world like other overarching theories of science can be tested is because Darwinian evolution does not have a rigid mathematical basis to test against as other overarching theories have. (in fact, in so far as math can be applied to Darwinian claims, mathematics constantly shows us that Darwinian evolution is astronomically unlikely),,

    “On the other hand, I disagree that Darwin’s theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?”
    – Berlinski, D., “A Scientific Scandal?: David Berlinski & Critics,” Commentary, July 8, 2003

    Darwinian Evolution is a Unfalsifiable Pseudo-Science – Mathematics – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1132659110080354/?type=2&theater

    Evolution is Missing a Mathematical Formula
    Excerpt: Virtually all scientists acknowledge that mathematics is the real language of science. Every theory uses words to describe and postulate the theory, but the true test of a theory is numbers and mathematics. It is numbers and mathematical formulae that distinguish true science from hocus-pocus.,,,
    Every scientific theory that has been promoted to the status of being a scientific law has been quantified and/or embodied into one or more mathematical formulae that make accurate predictions.
    But no scientist has been able to derive any working formula from the Theory of Evolution and no one has been able to quantify its dictums. Millions of scientists have tried to quantify the Theory of Evolution and they have all failed to do so.
    http://darwinconspiracy.com/article_1_rev2.php

    The reason why no scientist has been able ‘quantify its dictums’ is because there are no known laws of nature for Darwinists to appeal to to base their math on. In other words, there is no known ‘law of evolution’ in the physical universe:

    The Evolution of Ernst: Interview with Ernst Mayr – 2004
    Excerpt: biology (Darwinian Evolution) differs from the physical sciences in that in the physical sciences, all theories, I don’t know exceptions so I think it’s probably a safe statement, all theories are based somehow or other on natural laws. In biology, as several other people have shown, and I totally agree with them, there are no natural laws in biology corresponding to the natural laws of the physical sciences.
    http://www.scientificamerican......-ernst-in/

    WHAT SCIENTIFIC IDEA IS READY FOR RETIREMENT? Evolution is True – Roger Highfield – January 2014
    Excerpt:,,, Whatever the case, those universal truths—’laws’—that physicists and chemists all rely upon appear relatively absent from biology.
    Little seems to have changed from a decade ago when the late and great John Maynard Smith wrote a chapter on evolutionary game theory for a book on the most powerful equations of science: his contribution did not include a single equation.
    http://www.edge.org/response-detail/25468

    “It is our contention that if ‘random’ is given a serious and crucial interpretation from a probabilistic point of view, the randomness postulate is highly implausible and that an adequate scientific theory of evolution must await the discovery and elucidation of new natural laws—physical, physico-chemical, and biological.”
    Murray Eden, “Inadequacies of Neo-Darwinian Evolution as a Scientific Theory,” Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution, editors Paul S. Moorhead and Martin M. Kaplan, June 1967, p. 109.

  39. 39
    bornagain77 says:

    And whereas Darwinian evolution has no law of nature to appeal to so as to establish itself as a proper science, Intelligent Design does not suffer from such a disconnect from physical reality. In other words, Intelligent Design can appeal directly to ‘the laws of conservation of information’ in order to establish itself as a proper and rigorous science.

    Conservation of information, evolution, etc – Sept. 30, 2014
    Excerpt: Kurt Gödel’s logical objection to Darwinian evolution:
    “The formation in geological time of the human body by the laws of physics (or any other laws of similar nature), starting from a random distribution of elementary particles and the field is as unlikely as the separation of the atmosphere into its components. The complexity of the living things has to be present within the material [from which they are derived] or in the laws [governing their formation].”
    Gödel – As quoted in H. Wang. “On `computabilism’ and physicalism: Some Problems.” in Nature’s Imagination, J. Cornwall, Ed, pp.161-189, Oxford University Press (1995).
    Gödel’s argument is that if evolution is unfolding from an initial state by mathematical laws of physics, it cannot generate any information not inherent from the start – and in his view, neither the primaeval environment nor the laws are information-rich enough.,,,
    More recently this led him (Dembski) to postulate a Law of Conservation of Information, or actually to consolidate the idea, first put forward by Nobel-prizewinner Peter Medawar in the 1980s. Medawar had shown, as others before him, that in mathematical and computational operations, no new information can be created, but new findings are always implicit in the original starting points – laws and axioms.,,,
    http://potiphar.jongarvey.co.u.....ution-etc/

    Evolutionary Computing: The Invisible Hand of Intelligence – June 17, 2015
    Excerpt: William Dembski and Robert Marks have shown that no evolutionary algorithm is superior to blind search — unless information is added from an intelligent cause, which means it is not, in the Darwinian sense, an evolutionary algorithm after all. This mathematically proven law, based on the accepted No Free Lunch Theorems, seems to be lost on the champions of evolutionary computing. Researchers keep confusing an evolutionary algorithm (a form of artificial selection) with “natural evolution.” ,,,
    Marks and Dembski account for the invisible hand required in evolutionary computing. The Lab’s website states, “The principal theme of the lab’s research is teasing apart the respective roles of internally generated and externally applied information in the performance of evolutionary systems.” So yes, systems can evolve, but when they appear to solve a problem (such as generating complex specified information or reaching a sufficiently narrow predefined target), intelligence can be shown to be active. Any internally generated information is conserved or degraded by the law of Conservation of Information.,,,
    What Marks and Dembski (mathematically) prove is as scientifically valid and relevant as Gödel’s Incompleteness Theorem in mathematics. You can’t prove a system of mathematics from within the system, and you can’t derive an information-rich pattern from within the pattern.,,,
    http://www.evolutionnews.org/2.....96931.html

    Active Information in Metabiology – Winston Ewert, William A. Dembski, Robert J. Marks II – 2013
    Except page 9: Chaitin states [3], “For many years I have thought that it is a mathematical scandal that we do not have proof that Darwinian evolution works.” In fact, mathematics has consistently demonstrated that undirected Darwinian evolution does not work.,,
    Consistent with the laws of conservation of information, natural selection can only work using the guidance of active information, which can be provided only by a designer.
    http://bio-complexity.org/ojs/.....O-C.2013.4

    And since Intelligent Design is mathematically based on the ‘law of conservation of information’, that makes Intelligent Design testable and potentially falsifiable, and thus makes Intelligent Design, unlike Darwinism, a rigorous science.

    The Law of Physicodynamic Incompleteness – David L. Abel
    Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”
    If only one exception to this null hypothesis were published, the hypothesis would be falsified. Falsification would require an experiment devoid of behind-the-scenes steering. Any artificial selection hidden in the experimental design would disqualify the experimental falsification. After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided.
    The time has come to extend this null hypothesis into a formal scientific prediction:
    “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.”
    https://www.academia.edu/Documents/in/The_Law_of_Physicodynamic_Incompleteness

    It’s (Much) Easier to Falsify Intelligent Design than Darwinian Evolution – Michael Behe, PhD
    https://www.youtube.com/watch?v=_T1v_VLueGk

    “The National Academy of Sciences has objected that intelligent design is not falsifiable, and I think that’s just the opposite of the truth. Intelligent design is very open to falsification. I claim, for example, that the bacterial flagellum could not be produced by natural selection; it needed to be deliberately intelligently designed. Well, all a scientist has to do to prove me wrong is to take a bacterium without a flagellum, or knock out the genes for the flagellum in a bacterium, go into his lab and grow that bug for a long time and see if it produces anything resembling a flagellum. If that happened, intelligent design, as I understand it, would be knocked out of the water. I certainly don’t expect it to happen, but it’s easily falsified by a series of such experiments.
    Now let’s turn that around and ask, How do we falsify the contention that natural selection produced the bacterial flagellum? If that same scientist went into the lab and knocked out the bacterial flagellum genes, grew the bacterium for a long time, and nothing much happened, well, he’d say maybe we didn’t start with the right bacterium, maybe we didn’t wait long enough, maybe we need a bigger population, and it would be very much more difficult to falsify the Darwinian hypothesis.
    I think the very opposite is true. I think intelligent design is easily testable, easily falsifiable, although it has not been falsified, and Darwinism is very resistant to being falsified. They can always claim something was not right.”
    – Dr Michael Behe

    The Origin of Information: How to Solve It – Perry Marshall
    Where did the information in DNA come from? This is one of the most important and valuable questions in the history of science. Cosmic Fingerprints has issued a challenge to the scientific community:
    “Show an example of Information that doesn’t come from a mind. All you need is one.”
    “Information” is defined as digital communication between an encoder and a decoder, using agreed upon symbols. To date, no one has shown an example of a naturally occurring encoding / decoding system, i.e. one that has demonstrably come into existence without a designer.
    A private equity investment group is offering a technology prize for this discovery (up to 3 million dollars). We will financially reward and publicize the first person who can solve this;,,, To solve this problem is far more than an object of abstract religious or philosophical discussion. It would demonstrate a mechanism for producing coding systems, thus opening up new channels of scientific discovery. Such a find would have sweeping implications for Artificial Intelligence research.
    http://cosmicfingerprints.com/solve/

    Of related note: In so far as Darwinian evolution is dependent on materialistic premises, and regardless of whether Darwinists accept the falsification or not, Darwinian evolution is now currently being falsified by advances in quantum biology:

    Jim Al-Khalili, at the 2:30 minute mark of the following video states,
    “,,and Physicists and Chemists have had a long time to try and get use to it (Quantum Mechanics). Biologists, on the other hand have got off lightly in my view. They are very happy with their balls and sticks models of molecules. The balls are the atoms. The sticks are the bonds between the atoms. And when they can’t build them physically in the lab nowadays they have very powerful computers that will simulate a huge molecule.,, It doesn’t really require much in the way of quantum mechanics in the way to explain it.”
    At the 6:52 minute mark of the video, Jim Al-Khalili goes on to state:
    “To paraphrase, (Erwin Schrödinger in his book “What Is Life”), he says at the molecular level living organisms have a certain order. A structure to them that’s very different from the random thermodynamic jostling of atoms and molecules in inanimate matter of the same complexity. In fact, living matter seems to behave in its order and its structure just like inanimate cooled down to near absolute zero. Where quantum effects play a very important role. There is something special about the structure, about the order, inside a living cell. So Schrodinger speculated that maybe quantum mechanics plays a role in life”.
    Jim Al-Khalili – Quantum biology – video
    – youtube

    Molecular Biology – 19th Century Materialism meets 21st Century Quantum Mechanics – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1141908409155424/?type=2&theater

  40. 40
    Anaxagoras says:

    Interestingly, the next post at UD addresses Denton´s claim that discontinuity is pervasive in Nature.
    If this is so, who cares about common descent?
    What is the explanatory power of common descent concerning the origin of biological novelties?

  41. 41
    ThickPython says:

    @Andre, #35:

    You do know that common descent is just an assumption right?

    Not interested in playing word games. Common descent is a hypothesis that is supported by an enormous number of facts, and those facts are very difficult to be interpreted by any other model. If you want to say this still isn’t “proof”, then that’s fine, I’ll just presume (not assume!) that your burden of proof is so high that day-to-day life must be excruciating for you.

    “But there’s so much contradictory data!”, I hear you say. Well then maybe you could answer the challenge as well – do you believe that the shark-human-zebrafish article is a problem for common descent?

    It’s a test of both your understanding of common descent as well as your reasoning capability.

    #36:

    Keep it civil and stop throwing insults at people that disagree with you.

    I said please, didn’t I?

  42. 42
    bornagain77 says:

    “I’ll just presume (not assume!) that your burden of proof is so high that day-to-day life must be excruciating for you.”

    Any person who can so easily overlook the Cambrian explosion, and the fossil record in general, and not see a major problem for the hypothesis of common descent, is not really interested in whether common descent can ever be falsified or not but is only interested, IMHO, in protecting their personal religious views regardless of what the science is.

    What Types of Evolution Does the Cambrian Explosion Challenge? – Stephen Meyer – video – (The Cambrian Explosion directly challenges Universal Common Descent and the Mechanism of Random Variation/Natural Selection)
    https://www.youtube.com/watch?v=AaF7t5wRFtA&list=UUUMhP2x7_7psVO-H4MJFpAQ

    Dr. Stephen C. Meyer, PhD talks about the Case for Intelligent Design – video (excellent lecture on the Cambrian Explosion – Oct. 2015)
    https://www.youtube.com/watch?v=vl802lHAk5Y
    Oct 18, 2015 – Trinity Classical Academy’s Speaker Series welcomes Dr. Stephen C. Meyer, PhD, author of the New York Times® Bestseller Darwin’s Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design, and Signature in the Cell: DNA and the Evidence for Intelligent Design, which won “Book of the Year” by The Times of London Literary Supplement.

    “Darwin had a lot of trouble with the fossil record because if you look at the record of phyla in the rocks as fossils why when they first appear we already see them all. The phyla are fully formed. It’s as if the phyla were created first and they were modified into classes and we see that the number of classes peak later than the number of phyla and the number of orders peak later than that. So it’s kind of a top down succession, you start with this basic body plans, the phyla, and you diversify them into classes, the major sub-divisions of the phyla, and these into orders and so on. So the fossil record is kind of backwards from what you would expect from in that sense from what you would expect from Darwin’s ideas.”
    James W. Valentine – as quoted from “On the Origin of Phyla: Interviews with James W. Valentine” – (as stated at 1:16:36 mark of video)
    https://www.youtube.com/watch?v=xtdFJXfvlm8&feature=player_detailpage#t=4595

    Erwin and Valentine’s The Cambrian Explosion Affirms Major Points in Darwin’s Doubt: The Cambrian Enigma Is “Unresolved” – June 26, 2013
    Excerpt: “In other words, the morphological distances — gaps — between body plans of crown phyla were present when body fossils first appeared during the explosion and have been with us ever since. The morphological disparity is so great between most phyla that the homologous reference points or landmarks required for quantitative studies of morphology are absent.”
    Erwin and Valentine (p. 340)
    http://www.evolutionnews.org/2.....73671.html

    Scientific study turns understanding about evolution on its head – July 30, 2013
    Excerpt: evolutionary biologists,,, looked at nearly one hundred fossil groups to test the notion that it takes groups of animals many millions of years to reach their maximum diversity of form.
    Contrary to popular belief, not all animal groups continued to evolve fundamentally new morphologies through time. The majority actually achieved their greatest diversity of form (disparity) relatively early in their histories.
    ,,,Dr Matthew Wills said: “This pattern, known as ‘early high disparity’, turns the traditional V-shaped cone model of evolution on its head. What is equally surprising in our findings is that groups of animals are likely to show early-high disparity regardless of when they originated over the last half a billion years. This isn’t a phenomenon particularly associated with the first radiation of animals (in the Cambrian Explosion), or periods in the immediate wake of mass extinctions.”,,,
    Author Martin Hughes, continued: “Our work implies that there must be constraints on the range of forms within animal groups, and that these limits are often hit relatively early on.
    Co-author Dr Sylvain Gerber, added: “A key question now is what prevents groups from generating fundamentally new forms later on in their evolution.,,,
    http://phys.org/news/2013-07-s.....ution.html

    As to genetic sequences:

    “The genomic revolution did more than simply allow credible reconstruction of the gene sets of ancestral life forms. Much more dramatically, it effectively overturned the central metaphor of evolutionary biology (and, arguably, of all biology), the Tree of Life (TOL), by showing that evolutionary trajectories of individual genes are irreconcilably different. Whether the TOL can or should be salvaged—and, if so, in what form—remains a matter of intense debate that is one of the important themes of this book.”
    Koonin, Eugene V. (2011-06-23). The Logic of Chance: The Nature and Origin of Biological Evolution (FT Press Science) (Kindle Locations 76-80). Pearson Education (USA). Kindle Edition.
    more studies

    A New Model for Evolution: A Rhizome – Didier Raoult – May 2010
    Excerpt: Thus we cannot currently identify a single common ancestor for the gene repertoire of any organism.,,, Overall, it is now thought that there are no two genes that have a similar history along the phylogenic tree.,,,Therefore the representation of the evolutionary pathway as a tree leading to a single common ancestor on the basis of the analysis of one or more genes provides an incorrect representation of the stability and hierarchy of evolution. Finally, genome analyses have revealed that a very high proportion of genes are likely to be newly created,,, and that some genes are only found in one organism (named ORFans). These genes do not belong to any phylogenic tree and represent new genetic creations.
    http://darwins-god.blogspot.co.....izome.html

    Toward a Consensus: An Open Letter to BioLogos on the Genetic Evidence – Cornelius Hunter – May 27, 2016
    Excerpt: One of Venema’s basic points (see here and here) is that the genomes of different species are what we would expect if they evolved.,,,
    What Does the Evidence Say?
    For starters, phylogenetic incongruence is rampant in evolutionary studies. Genetic sequence data do not fall into the expected evolutionary pattern. Conflicts exist at all levels of the evolutionary tree and throughout both morphological and molecular traits.,,,
    As one evolutionist explained, “The tree of life is being politely buried.”,,,
    http://www.evolutionnews.org/2.....02879.html

    Logged Out – Scientists Can’t Find Darwin’s “Tree of Life” Anywhere in Nature by Casey Luskin – Winter 2013
    Excerpt: the (fossil) record shows that major groups of animals appeared abruptly, without direct evolutionary precursors.
    Because biogeography and fossils have failed to bolster common descent, many evolutionary scientists have turned to molecules—the nucleotide and amino acid sequences of genes and proteins—to establish a phylogenetic tree of life showing the evolutionary relationships between all living organisms.,,,
    Many papers have noted the prevalence of contradictory molecule-based phylogenetic trees. For instance:
    • A 1998 paper in Genome Research observed that “different proteins generate different phylogenetic tree[s].”6
    • A 2009 paper in Trends in Ecology and Evolution acknowledged that “evolutionary trees from different genes often have conflicting branching patterns.”7
    • A 2013 paper in Trends in Genetics reported that “the more we learn about genomes the less tree-like we find their evolutionary history to be.”8
    Perhaps the most candid discussion of the problem came in a 2009 review article in New Scientist titled “Why Darwin Was Wrong about the Tree of Life.”9 The author quoted researcher Eric Bapteste explaining that “the holy grail was to build a tree of life,” but “today that project lies in tatters, torn to pieces by an onslaught of negative evidence.” According to the article, “many biologists now argue that the tree concept is obsolete and needs to be discarded.”,,,
    Syvanen succinctly summarized the problem: “We’ve just annihilated the tree of life. It’s not a tree any more, it’s a different topology entirely. What would Darwin have made of that?” ,,,
    “battles between molecules and morphology are being fought across the entire tree of life,” leaving readers with a stark assessment: “Evolutionary trees constructed by studying biological molecules often don’t resemble those drawn up from morphology.”10,,,
    A 2012 paper noted that “phylogenetic conflict is common, and [is] frequently the norm rather than the exception,” since “incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species.”12,,,
    http://www.salvomag.com/new/ar.....ed-out.php

  43. 43
    HeKS says:

    Prof. Swamidass @33

    You said:

    You are correct. Proving this lncRNA function is not easy, especially because there is no obvious evidence that it is functional.

    Unfortunately, the onus is on those that claim this lncRNA is functional to prove it. The current understanding of biology is that 99% of lncRNA’s are non-functional. In fact, 98% are not even expressed at more than 1 copy per cell, as far as we can tell.

    To me, this is a great example of the problematic thinking that derives from Methodological Naturalism, which, in biology, rules out agent causation.

    In any other scenario, someone working with a digital code controlling complex functionality would begin with the assumption that any given block of code has a purpose and that the burden of proof would rest on anyone who wanted to assert that the vast majority of the code was functionless.

    As a programmer, I would say that the default assumption of non-function makes no sense, nor does the methodology and logic used to conclude a block of code is non-functional strike me as remotely convincing. If someone came up to me and told me that a huge portion of a complex piece of software code served no purpose, I would ask them why they thought that. If they responded by telling me that it was because they had been watching the execution of the compiled binary code and huge chunks of it were never being run, even after running the program thousands and thousands of times, I would facepalm so hard I might knock myself unconscious.

    You also said:

    Once again, if we reject common descent, why do we have this broken gene? What design principle explains this pattern?

    Maybe CD + design is a good possibility, but design alone does not explain this.

    Am I correct in understanding you to be saying that design alone does not explain this because you think this is non-functional code?

  44. 44
    ThickPython says:

    @HekS, #43:

    As a programmer …

    I’m a programmer as well, and I’ve got code currently in a production system that – if it were run – would crash the system. Obviously it still compiles, but it doesn’t mean it makes sense for that code to be there. It just happens to be code that I wrote a long time ago that worked at the time, and now it doesn’t …

    … kinda like how the vitellogenin gene worked a long time ago, but now it does nothing and all that’s left is a relic.

  45. 45
    Andre says:

    ThickPython

    Not interested in playing word games. Common descent is a hypothesis that is supported by an enormous number of facts, and those facts are very difficult to be interpreted by any other model. If you want to say this still isn’t “proof”, then that’s fine, I’ll just presume (not assume!) that your burden of proof is so high that day-to-day life must be excruciating for you.

    It is still an assumption, don’t forget that 🙂

    “But there’s so much contradictory data!”, I hear you say. Well then maybe you could answer the challenge as well – do you believe that the shark-human-zebrafish article is a problem for common descent?

    Perhaps you’re not familiar with my position on CD, I’ll help you. I am not opposed to CD, I’m just not convinced by it yet, as the evidence is circumstantial at best and common design explains it as easily. You are of course welcome to claim your allegiance to CD as some irrefutable fact, myself not yet, I need more verifiable evidence for that, thanks.

    I said please, didn’t I?

    It’s not your please that is the issue here. It’s your poisoning the well….. FYI; Dwayne Gish has never lost a debate to a Darwinist, so when you equate BA with the old Gish Gallop, please take note its considered a backhanded compliment to those that care about truth.

  46. 46
    Origenes says:

    HeKS #43,#26.

    I would like to add that — unlike a computer — an organism can perform miracles with what is still available to it. At the macro level Slijper’s goat is a good example. The other day my physiotherapist informed me that one of the four muscles in the rotator cuff of my left shoulder was missing. To his surprise he was unable to discern loss of shoulder function.

  47. 47
    Peer says:

    “The vast majority of lncRNAs are not important; they merely express noise.”

    This is anti-science, similar to “junk DNA”. Be reminded that a huge number of protein-coding genes seem not important, they turn out to be redundant as they operate in networkss. Are they merely expression noise? People who claim so, do not understand biology. Thinking about redundancy…pleiotropy springs in mind.

    Vitellogenin genes are not only involved in yolk formation…they are also function as anti-oxidants. With many anti-oxidant genes in the genomes (dozens) and many anti-oxidants (vitamines) taken up by food, single anti-oxidant genes are more or less redundant and not subject to natural preservation. The fate of redundant genes (here: vitellogenin genes) is inactivation and loss through an accumulation of mutations.

    The genomes were frontloaded with al sorts of handy information (genetic elements, genes, regulatory elements, insulators, VIGEs, etc). Evolution is nothing but shuffling of these elements. The environment determines what part is preserved and in what context (natural preservation). Frontloaded evolution is the only viable theory.
    (read my papers published in JoC)

  48. 48
    Andre says:

    I can’t help but harp on this but cladistics rests on 3 assumptions. It is very important to me that we discern between assumptions and facts. Unless there is compelling evidence and I really don’t mean a few genes and some physical similarities I remain agnostic or slightly bias against these assumptions…..

    I think this is really important because Common descent as argued in the paper I’m linking is considered a fundamental tenet of evolutionary biology and in this case we know they mean Darwinian evolutions. The problem is this theory has simply not been able to demonstrate its core argument.

    http://mail.ypu.edu.tw/~wnhuan.....ics/14.pdf

  49. 49
    Peer says:

    The problem with Venema — common descent believers in general — is the always-verifying-mode of the concept. This, while genuine science would rather falsify a certain proposition. If we take the latter as a lead, and we look at the genomes of…say… humans and chimp, we observe 2000-3000 unique protein-coding- and miRNA-genes setting the organisms apart. This defies common ancestry of humans and chimps by a random evolutionary mechanism.
    The real problem is, of course, that evolutionary theory (E) cannot be falsified at all, because shared traits proof common descent (CD), whereas unique characteristics proof evolutionary modifcations (M). Thus, E=CD+M (Darwinism) is unscientific and can only qualify as pseudoscience.

  50. 50
    bill cole says:

    Dr Swamidass

    To be very clear, I am claiming that this is a NON-functional lncRNA because there >98% of lncRNAs are functional and no evidence has been presented that indicates that this specific lncRNA is functional.

    So the math is easy. (1) start with a functional VTG1 gene. This gene is being transcribed into RNA and then translated into protein. (2) mutate this gene so we BREAK its ability to be translated. There should be no debate here, ID has not problem with the notion that mutations can break things, right.

    If you tried to model this mathematically I think it would not be easy but certainly to get one would be within the resources of populations and generations. I think you then agree to get a functional lncRNA would beyond evolutionary resources.

    Regarding the fusion debate the most problematic issue is the discovery of a gene at that location. The counter argument you provided does acknowledge the existence of the gene. In my mind this is an absolute show stopper for this evidence supporting common decent based on the sequential space of the genome. To get a gene there requires an intelligent agent or some mechanism no one has thought of yet.

    A good topic for dinner in July 🙂

  51. 51

    @50

    Functional lncRNA is possible too, but that takes more time to explain. Dinner conversation it is.

    You better email me soon. Plans are filling up already.

  52. 52
    HeKS says:

    @ThickPython #44

    Hi ThickPython,

    You said:

    I’m a programmer as well, and I’ve got code currently in a production system that – if it were run – would crash the system. Obviously it still compiles, but it doesn’t mean it makes sense for that code to be there. It just happens to be code that I wrote a long time ago that worked at the time, and now it doesn’t …

    … kinda like how the vitellogenin gene worked a long time ago, but now it does nothing and all that’s left is a relic.

    I don’t think you’re quite getting my point.

    First of all, you’re operating on the premise that this section of code in humans is definitely non-functional, which is precisely the thing I’m saying is very, very difficult to determine and should not be our default position from a practical perspective. Then, operating on that premise (that this section of code in humans is non-functional), you’re making a comparison to an obsolete block of code in a piece of software that hasn’t been removed.

    There can be no doubt that this sort of thing happens, but the question is this: How do you know that the code is obsolete?

    If you personally wrote the code at every step then you might immediately know that you’ve replaced this section of code with something more recent and so this old block of code is unnecessary. Perhaps you had even commented it out. If, on the other hand, you were coming into a project where the software had been built by someone else, you would typically have to go through a more rigorous process to determine that some block of code was unnecessary (though modern coding tools can make this easier to determine).

    Regardless of which of these scenarios happens to be the case, there are at least two points that need to be appreciated:

    1) The fact that the code is no longer necessary does not mean that it is inherently non-functional. In other words, it’s not just gibberish or a series of randomly generated characters. Nor is it likely even code that has somehow been corrupted by a typo or improper syntax. In most cases, the code itself would be inherently functional and could still function when placed into an appropriate context. It is actually the overall context that has made the block of code unnecessary, not a lack of inherent functionality in the code itself.

    And even more importantly…

    2) We are able to establish that the block of code is unnecessary because we can read and understand it, both on its own and in its larger context. This is extremely important, and this is just what we can’t do with DNA.

    DNA operates like software, but it is obviously not like any readable programming language. It is more like a piece of programming that has been compiled to machine code. We can get a sense of what blocks of code do by observing the results of that block being expressed, but this is very different from having the ability to directly read and fully interpret the code itself.

    Now, imagine you are asked to sit in front of a monitor and watch a display of binary code being run over and over. As you watch, you notice that big chunks of 1’s and 0’s are never actually being executed. After several hours of watching this code run, someone comes up to you, dumps a million dollars on the table in front of you, and tells you that you must use this money to make a bet on whether these large sections of code that are not being executed are purposeful or purposeless, and you get to keep the money if you’re right (you can substitute a gun to your head if you like). Which one do you choose?

    I can tell you right now that I’d choose purposeful every time. Why? Because I know that I could write an application today, following best practice design patterns, in which every line of code is purposeful, and yet, not only would the bulk of that code never be expected to run, but I would actually hope that it would never run. Indeed, it would not be at all unusual for the functional code that is actually expected to be executed during a session to be dwarfed by the functional code that is generally not expected to be executed.

    Now, if we know this to be the case with intelligently designed software – namely, that a vast majority of the code in a piece of software may not and likely will not be executed under normal conditions even though all of that unexecuted code is functional and purposeful – why would we assume the opposite when it comes to DNA software, unless we are starting with the assumption that DNA is not the product of intelligent design and is instead the product of a mindless and purposeless process? (BTW, I have no idea where you stand on the issue of ID)

    Take care,
    HeKS

  53. 53
    aap says:

    As a multiyear watcher on UD I have appreciated the discussions and the willingness of ID scientists, computer programmers, philosophers, engineers, lawyers and others who enjoy thinking for themselves and are willing to take the flak in challenging methodological naturalistic evolutionary orthodoxy. I believe that theistic evolution is bad science and very bad theology. I won’t get into the bad theology part, which is nothing more than a poisonous liberal recipe of Esau’s bowl of pottage which has been slowly and painfully destroying the mainline churches and is now invading the evangelical churches. Forget the theology for now, the science is wanting. For over the past 45 or so years since becoming interested in the evolution-creation debate I have heard a lot of huffing and bluffing on the part of evolutionists, theistic or otherwise, of “we are going to blow your creationist house down with all of the overwhelming evidence for common descent via the materialistic evolutionary process”. The present issue on this thread regarding vestigial genetic markers and the “God wouldn’t do it this way” comments are, as others have pointed out, just a regurgitating of the older vestigial organ arguments which didn’t turn out very well for the evolutionary believers. Like many others I have been waiting and watching for some real hard evidence that actually supports the evolutionary beliefs. I think it is time for evolutionists, theistic or otherwise, to either put up or shut up. My challenge for Drs. Venema and Swamidass and other evolutionists is to show us the goods, let us see “the money”. Most biological evolutionists, theistic or otherwise, give the impression that they are experts in their understanding of the evolutionary mutational and natural selection process. In their superior knowledge they tell us that they understand and can see how common descent works. So I say, show us what you can do with your evolutionary knowledge. How about something simple like creating a new cellular life form from non-life. If they believe that life happened by accidental processes, why don’t they give us a demonstration or least an explanation of how those kind of accidents can happen, and why they don’t keep happening. Or, is it just part of their belief system? Despite all of the hype in OOL research, they are light years away from understanding what life actually is, let alone being able to manufacture it from non-life. Today, through real scientific disciplines we know that all life forms are information rich with irreducibly complex and integrated miniature computerized type systems. Real science teaches us that life doesn’t come from non-life, but all life comes from the “Word”- the information created by the Creator. Why don’t the evolutionary biologists use their “superior knowledge” and give us a demonstration of the power of the evolutionary process. Where are all of the peer reviewed papers explaining to us “duffusses” exactly which mutations have to take place in order to transform one kind of creature into another and how those mutations were caused. How about changing a unicellular life form into a different kind of viable multicellular life form through the application of directed mutations and natural selection. That shouldn’t be too hard with all of their expertize. No, all they have managed to do with their extensive knowledge of evolution and years of experimentation and wasted government funding of evolutionary biology is to produce either deformed or dead bacteria or houseflies. Where would evolutionary biology be without government welfare? Who is going to waste their own money on research that doesn’t produce any concrete results? How about something a little more challenging like transforming an asexual lifeform into a sexually reproducing life form. Let them show us how it happens. Now if they really are smart they will also be able to create sentient life through accidental mutations. I am waiting, and so are many others. True science can create some amazing technological contraptions which are almost miraculous, but only GOD can do what is truly miraculous, which is the creation of our universe and every kind of life, including human life.
    It is time to end the huffing and bluffing and just-so stories and speculations about vestigial organs or genetics and give us the real deal. Professor Richard Lewontin, a geneticist and one of the world’s leaders in evolutionary biology, wrote this very revealing statement that highlights the implicit a priori bias against GOD that he and many other methodological naturalistic scientists hold:
    ‘We take the side of science in spite of the patent absurdity of some of its constructs, in spite of its failure to fulfill many of its extravagant promises of health and life, in spite of the tolerance of the scientific community for unsubstantiated just-so stories, because we have a prior commitment, a commitment to materialism. It is not that the methods and institutions of science somehow compel us to accept a material explanation of the phenomenal world, but, on the contrary, that we are forced by our a priori adherence to material causes to create an apparatus of investigation and a set of concepts that produce material explanations, no matter how counter-intuitive, no matter how mystifying to the uninitiated. Moreover, that materialism is an absolute, for we cannot allow a Divine Foot in the door.’

    Yes, the Divine Foot feared by Richard Lewontin and other materialistic minded scientists is not only in the door but is trampling on their cherished evolutionary religious beliefs that they are nothing more than mutated and mutating creatures who are free from the Divine will.
    Lastly, it is tragic that theistic evolutionists in their insistence on methodological naturalism usually take the side of the scientific establishment in the ostracizing and persecution of other scientists who do not believe the evidence supports evolutionary common descent, but instead points to an Intelligent Designer or Creator GOD. It is understandable why atheistic believers would hold to evolutionary beliefs and not be able to see the power and wisdom of GOD revealed in His Creation, for they have nothing else but evolution to believe in, but it is lamentable that those who express theism should be so blind as not to see GOD’S hand in His absolutely incredible handiwork in the universe and in life, particularly human life. It is time for all scientists to humble themselves and give GOD the glory He deserves for His miraculous creations. ID is a good start.

  54. 54
    Dr JDD says:

    @12:

    @8 lncRNAs are only rarely important. This paper is a good overview (no paywall): http://www.ncbi.nlm.nih.gov/pm…..MC4306305/

    “Although the estimated number of different types of human lncRNAs has ranged from 5,400 to 53,000 (Table ?Table22), only a small fraction have been found to be present at levels high enough to suggest that they have a function. According to ENCODE’s own estimates, fewer than 1,000 lncRNAs are present at greater than one copy per cell in the typical human tissue culture cell line (Djebali et al., 2012; Palazzo and Gregory, 2014), although some other estimates have determined that the levels may be substantially higher (Hangauer et al., 2013)”

    To be clear, of the 1,000 lncRNAs that are expressed above 1 copy per cell (<2% of lncRNAs), very few have been demonstrated to be functional. Moreover, lncRNAs are very easy to generate by mutation, so even those that are functional in cancer may very well be de novo lncRNAs that are not part of the normal function of normal human cells.

    You mean the review written by the biochemist at Toronto university (ring any bells for another avid pro-junker) and the author of the review article "The case for junk DNA"? Well that won't be biased at all towards the non-functionality of non-coding regions and maintaining that the majority of the genome is junk…..

    OK, that's an ad hominem but my underlying point remains – there are many other researchers indifferent to the needs (yes, needs) of evolutionary biology to hold onto the non-functionality and junk status of the majority of the human genome and they have no problem with the idea that many lncRNA's provide function. (my point is that this is one review with one point of view and many others actively working in this area are likely to disagree)

    A couple of points to make:
    1) Number of transcripts per cell is a misnomer. There are plenty of examples where when you take even an apparent clonal cell line population and work out the number of transcripts that it can come up as very low, but that is because it is a population based number. To put it more simply, if you have 100,000 cells and 100 of those are in a certain cell cycle stage when you lyse them to extract the RNA, that means that you would need 1000 copies of a particular RNA in each of those 100 cells in order to average out at 1 copy per cell. But that average would be meaningless as it only tells you about a population. One of the biggest growing areas (and trendiest) of activity in the medical field and cell biology is single cell analyses as people are starting to understand how different even apparently "same types" of cells are from one to another. This can be useful for example in understanding how a patient may respond to a drug and which cells are important in that response. Only recently is this technology avaialble with the likes of single cell sorting, single cell PCR and single cell transcriptome analysis. I wonder, when this analysis was performed to state that most lncRNAs are at 1 or less copy per cell, was this a population analysis or at the level of single cells? Did it analyse developmental stages or, was it mainly based on cells sitting in a flask?

    2) The growing body of evidence about misregulation of lncRNAs in disease is indicative of potential roles. For example, many tumours appear to have misregulation of lncRNAs and this is important for properties such as proliferation, invasion, division, etc. This suggests that as these types of events are more pronounced in devlopment, embryogenesis and unique subsets of cells in the adult, that their expression may likely to be low in an average cell and tightly regulated. Thus this would decrease the likelihood again of seeing these transcripts in a population basis.

    For some other reviews on lncRNAs for those interested, see:

    http://www.ncbi.nlm.nih.gov/pubmed/27254479
    http://www.ncbi.nlm.nih.gov/pubmed/27230909
    http://www.ncbi.nlm.nih.gov/pubmed/27163185

    http://www.ncbi.nlm.nih.gov/pubmed/27007508
    From the above link I quote:

    Recent findings implicate lncRNAs as key players of cellular differentiation, cell lineage choice, organogenesis and tissue homeostasis.

    Again, this is in-line with my above statement that if you assess a population of cells growing on a dish, it is unlikely you will see much of a piece of RNA important in cell differentiation, lineage choice, organogenesis…etc.

    This one in particular is of interest, for another perspective and potential role:
    http://www.ncbi.nlm.nih.gov/pubmed/27259198

    3) It is funny how the onus is on people now to prove function. The starting assumptions of biology really has changed over the years! Many years ago the motivation to study things of biology was teleological – there is a reason why something is the way it is. Then naturalism muscled that curiosity out of the cat and we now have a scenario where the base assumption is that most things are functionless or purposeless. But that is an evolution-driven mindset, which again speaks to my point above about how those not concerned with that side of research or rather the implications of it and the genome, are far and wide describing and celebrating functionality of things once erroneously assumed to be functionless, based on a false assumption, but driven by the need for them to be functionless. My approach to science has always been that things are there for a reason and they serve a purpose. Personally I have always found this approach has worked out well for me. And it is funny over the years to see the goalposts shift. When I started out I was being taught as an undergraduate that 99% of the genome was junk and functionless. Now it is down to maybe 90%. That is a pretty big change. All of the arguments I see here were used when that figure was at 99%. Give it time. Function will be found (prediction).

    Which leads me onto
    4) Limitations of current technologies. Granted we have made huge advances in technology and what we can do. EVen down as I have already drescribed to single cell analysis from phenotype to transcriptome analysis. But we still cannot (and should not) take a human embryo, CRISPR out a lncRNA and see what happens in development. We still cannot easily assess how other stimuli and complex cellular states affect expression of various genes and pieces of DNA. Indeed, when researchers expose Drosophila to stress, alcohol, and various other states they see uncharacterised genes and expression patterns emerge. Yet we look at some cells in a culture dish in a 2-d non-ECM containing environment and say that this represents what is going on in a complex organism. That is flawed. For me, the onus is not on those who suggest there may be function for an RNA, but rather, that is what science should seek out to investigate rather than instantly dismiss it in an assumptive matter as being irrelevant.

    Finally:
    5) I always find it supremely hilarious how evolution can account for a complex eye multiple independent times by random chance (convergence), can (just because food decides to grow higher) account for an incredible complex animal such as the giraffe with such distinct needs, but cannot get rid of a bit of junk DNA and stop it from being transcribed once it is broken (yet avoid somehow its translation).

    God is laughing at the wisdom of man!

    (All the above is of course, my own opinion and part of the debate. I accept I am likely wrong on many things.)

  55. 55
    PaV says:

    Prof. S. Joshua Swamidass:

    I’ve already asked this question:
    Where did the first bird feather come from?

    No one, but Mung, has answered. This simple question demolishes your entire argument unless you have an apt answer for it. I’d ask you to make some attempt to address this issue.

    You say that the presence of a chicken egg psuedogene in the human genome is proof of CD. Well, I say that the sudden, abrupt, and immediate production of the bird feather indicates a huge discontinuity in what you purport to be CD. Who’s right?

    Next, you’ve written:

    You are correct. Proving this lncRNA function is not easy, especially because there is no obvious evidence that it is functional.

    Unfortunately, the onus is on those that claim this lncRNA is functional to prove it. The current understanding of biology is that 99% of lncRNA’s are non-functional. In fact, 98% are not even expressed at more than 1 copy per cell, as far as we can tell.

    I will say, there might even be a Nobel Prize in it for someone who can demonstrate that most lncRNAs are functional. That would so overturn our current understanding of how biology works that the committee would likely take notice.

    Coming back down to earth, absent any additional evidence this putative lncRNA is most likely non-functional. From a CD perspective, it is most likely a leftover remnant of the previously functional VTG1 gene, or even just “noisy” gene expression and not a lncRNA. Certainly not anything that makes us doubt that that humans have an egg pseudogene in our genomes.

    Once again, if we reject common descent, why do we have this broken gene? What design principle explains this pattern?

    All this talk (bolded sentence) of “leftover remnant” and “previously functional” sounds just like the “junkDNA” argument that is now under attack. Why? Because function is being found everywhere.

    You run the risk of taking the wrong side of this argument.

    Here’s an article to look at.

    Evolutionary conservation of long non-coding RNAs; sequence, structure, function.
    Johnsson, Lipovich, Grandér, Morris KV

    BACKGROUND:
    Recent advances in genomewide studies have revealed the abundance of long non-coding RNAs (lncRNAs) in mammalian transcriptomes. The ENCODE Consortium has elucidated the prevalence of human lncRNA genes, which are as numerous as protein-coding genes. Surprisingly, many lncRNAs do not show the same pattern of high interspecies conservation as protein-coding genes. The absence of functional studies and the frequent lack of sequence conservation therefore make functional interpretation of these newly discovered transcripts challenging. Many investigators have suggested the presence and importance of secondary structural elements within lncRNAs, but mammalian lncRNA secondary structure remains poorly understood. It is intriguing to speculate that in this group of genes, RNA secondary structures might be preserved throughout evolution and that this might explain the lack of sequence conservation among many lncRNAs.
    SCOPE OF REVIEW:
    Here, we review the extent of interspecies conservation among different lncRNAs, with a focus on a subset of lncRNAs that have been functionally investigated. The function of lncRNAs is widespread and we investigate whether different forms of functionalities may be conserved.
    MAJOR CONCLUSIONS:
    Lack of conservation does not imbue a lack of function. We highlight several examples of lncRNAs where RNA structure appears to be the main functional unit and evolutionary constraint. We survey existing genomewide studies of mammalian lncRNA conservation and summarize their limitations. We further review specific human lncRNAs which lack evolutionary conservation beyond primates but have proven to be both functional and therapeutically relevant.
    GENERAL SIGNIFICANCE:
    Pioneering studies highlight a role in lncRNAs for secondary structures, and possibly the presence of functional “modules”, which are interspersed with longer and less conserved stretches of nucleotide sequences. Taken together, high-throughput analysis of conservation and functional composition of the still-mysterious lncRNA genes is only now becoming feasible.

    In answer to your demand for “proof,” the boldened text suggests that the RNA secondary structure is what is truly vital. It appears, from a very quick look at the literature, that lncRNA is very likely involved in chromosome duplication, where its physical structure alone might be vital.

    Due caution is needed here. You, along with Larry Moran, might end up with a whole lot of “egg” on your face. (pun intended!)

  56. 56
    CLAVDIVS says:

    aap @ 55

    Survey says: Young people are leaving the Christian church in droves, and amongst the top reasons is their perception that “churches are out of step with the scientific world we live in” and that “Christianity is anti-science”. Amongst young church leavers, 23% said they have “been turned off by the creation-versus-evolution debate.”

  57. 57
    CLAVDIVS says:

    Dr JDD

    5) I always find it supremely hilarious how evolution can account for a complex eye multiple independent times by random chance (convergence), can (just because food decides to grow higher) account for an incredible complex animal such as the giraffe with such distinct needs, but cannot get rid of a bit of junk DNA and stop it from being transcribed once it is broken (yet avoid somehow its translation).

    Haven’t scientists discovered that junk DNA has virtually zero fitness cost for large organisms? This is the opposite of gross features like eyes or necks where, if favoured by the environment, not having them has a big fitness cost. That would explain the situation without hilarity.

  58. 58
    aap says:

    Clavdivs at 56 Interesting survey. It is not surprising that those who have been fed and watered at the evolution trough through the public education systems are going to believe that the church is out of step with the rest of the world, just as they think that much of the church is out of step with the world on many other social issues, which of course the church should be. The public education systems are ambassadors of the world so it isn’t shocking that their graduates would be turning to the world instead of CHRIST. Many youth are looking for excuses for following the temptations of the world and the science- religion warfare thesis is a good excuse for them to use. The reality is they do not know CHRIST and His teaching. By the way do your own survey of the mainline liberal churches who adopted theistic evolution two, three, four generations ago: how many youth are left in them? Most of them are looking more and more like nursing homes and keeping the funeral homes busy.

  59. 59
    Origenes says:

    CLAVDIVS: Haven’t scientists discovered that junk DNA has virtually zero fitness cost for large organisms?

    Not having “junk DNA” would have an enormous fitness cost. Actually scientists (ENCODE) have been discovering more and more function for “junk DNA”.

    CLAVDIVS: This is the opposite of gross features like eyes or necks where, if favoured by the environment, not having them has a big fitness cost.

    Tell that to bacteria. Besides, what is favoured by the environment, does not explain the coming into existence of eyes and necks.

    CLAVDIVS: That would explain the situation without hilarity.

    Natural selection explains what is not, not what is.

    What Darwin called natural selection is actually a process of elimination.
    [Ernst Mayr]

  60. 60
    vjtorley says:

    Hi everyone,

    Some readers have suggested various functions for lincRNAs, but it’s worth putting these proposals in context. I quoted Larry Moran in my OP, because regardless of whether you agree with his views on evolution, he has a solid command of the literature relating to the junk DNA controversy. The following quotes from his posts should prove helpful.

    Remember: the onus is on us to demonstrate that most of these lincRNAs actually have a function.

    http://sandwalk.blogspot.ca/20.....lease.html

    It’s the lincRNAs and other noncharacterized RNAs that represent the biggest problem because if all of them have a function then there will be >50,000 genes in the human genome instead of the current estimates of about 25,000 (20,000 protein-coding genes and 5,000 genes for functional RNAs). If all of those RNAs were functional they would occupy about 1% of the genome so this has has very little to do with whether 90% of our genome is junk.

    http://sandwalk.blogspot.ca/20.....lease.html

    The authors [Blencowe et al.] did detect a few interactions involving long noncoding RNAs (lincRNAs) but this was only a small percentage of the total. There are thousands of lincRNAs but currently there are only about 200 that have known functions and not all of these are even human.

    http://sandwalk.blogspot.ca/20.....crnas.html

    As a general rule, these RNAs are longer than 200 bp and some scientists put the cutoff at 1000 bp. Simple eukaryotes, such as yeast, don’t have a lot of lncRNAs but eukaryotes with large complex genomes that are full of junk DNA seem to have a lot of different lncRNAs. The DNA regions that specify these lncRNAs are not conserved. This strongly suggests that many of the lncRNAs are spurious nonfunctional transcripts even though some of them have well-characteized functions [see On the function of lincRNAs].

    As usual, we have a definition problem. Are “lncRNAs” just a generic class of long noncoding RNAs that include thousands of nonfunctional molecules that are nothing more than junk RNA? Or, does the term “lncRNA” refer only to the subset that has a function? If it’s the latter, then we should probably be referring to “putative” lncRNAs most of the time since the vast majority have not been shown to have a function. (There are about 10,000 of these RNAs in humans.)

    I don’t see how you can avoid the elephant in the room whenever you talk about lncRNAs. The most important question in NOT whether some of them have a function — that was demonstrated 30 years ago. The important question is whether the majority, or even a substantial minority, have a function.

    http://sandwalk.blogspot.ca/20.....crnas.html

    Some of the most interesting RNAs are the long intergenic noncoding or lincRNAs (Ponting et al. 2009). The average size of these longer RNAs is about 1500 bp and there are about 1600 conserved lincRNA genes in the mammalian genome (Guttman et al., 2009). This makes up only about 0.08% of the genome but these RNAs are very curious.

    http://sandwalk.blogspot.ca/20.....crnas.html

    Hmmm … if you read my earlier post you’ll recall that even if all 3,000 transcripts were functional lncRNAs this would only account for about 0.1% of the genome. You would need hundreds of similar studies to make a significant dent in the amount of junk DNA, currently estimated to be 90% of the genome.

    Along the way, you would have to refute hundreds of published papers showing that most of our genome is junk.

    http://sandwalk.blogspot.ca/20.....iting.html

    Sloppiness might, by accident, lead to new genes but that’s not why things are sloppy. If having junk DNA were a clear advantage for future evolution then the genomes of all extant lineages should have lots of junk DNA and should make lots of lncRNAs.

  61. 61
    butifnot says:

    Swami et all – You don’t even know, what you don’t know. Your talk is as someone who has done the thing they are commenting on, you know, created life. It is clear there are VAST unknowns of control, timing, organization etc necessary to account for life that we are as yet unaware of. Yet glib proclamations about functionality or purpose abound. Comments thus far have done a nice job of highlighting foundational, mechanistic, logical, grossly assumptive … areas of serious trouble this UCD house of cards is built on. And it just seems like UCD – universal condescending demeanor – cannot be hidden by any amount of cordiality.

  62. 62

    It is remarkable to me how opinionated everyone is about an obscure detail of biology: lncRNAs. I wonder how many here have even heard of lncRNA’s before they encountered it in the ID debate (either here or somewhere else).

    How many of you actually care about lncRNAs beyond their role in the argument against evolution?

    I’ve been studying (without regard to evolution) for YEARS. You can disagree with biologists, but we do not come to our assessment of lncRNAs because of how it plays out in the ID debate. We do so because we really care to understand how they work. We have reasonably settled understanding of it now, and if that understanding were to change dramatically there would probably be a Nobel Prize granted for it.

    For the purpose of the ID debate, VJ’s quote of Moran is salient:

    “I don’t see how you can avoid the elephant in the room whenever you talk about lncRNAs. The most important question in NOT whether some of them have a function — that was demonstrated 30 years ago. The important question is whether the majority, or even a substantial minority, have a function.”

    Sure, a tiny number of lncRNA are functional. I said that from the beginning. All evidence suggests, however, the vast majority are NOT functional. Even all of the debate about lncRNA in the literature affirms this quote by Moran. If you do not believe me, just email some of the biologists writing the papers you are quoting, point them to the VTG1 lncRNA ask them if they think that specific lncRNA is functional. If they think it is functional, ask them why, and how they would demonstrate it. You will find >95% of them will agree with the assessment I have given you; the VTG1 transcript is 99% likely to be a non-functional lncRNA.

    Rather than quote mining, and constantly trying to argue one lncRNA’s function is proof that ALL have function, you have to start by understanding biology in its own terms. There is very good evidence that suggests most lncRNAs are non-functional. The only disagreement I know of among biologists is how important a small minority are in narrow circumstances (usually disease) or how important engineered (i.e. as a drug alternative) lncRNAs could be for treating disease.

    If you still persist in disagreeing with biologists, the onus is on you. Frankly, you will probably need to go get a PhD, start a lab, get some grants, and come back to me after 10 years of dedicated scientific work to convince us on this point. If you were successful, you might even become famous. Of course, none of you are going to do that, because most of you could care less how lncRNAs function, other than to use them as a rhetorical club against evolution.

    Once again, it is amazing to me how opinionated everyone is about lncRNAs. Other than ID, do you even care at all about how they function? Do you even know their mechanism of action?

    This might be surprising to you, but biologists are not really concerned about arguing against ID. They are focused on much different things, like understanding cancer, or different mechanisms in cells. We do biology to understand biology, not to argue for or against ID. I understand you guys care a lot about ID, but outside of design, do you care about biology at all?

    Honestly, it feels a objectifying.

    And, to be clear, I have no fear of being on the wrong side of the argument here. Frankly, I am not in an argument. Biology is not litigated in comments to blog posts. I’m here because I genuinely want to explain to the public how Biology actually works. I’m happy to explain to you how the experts understand it. It is clear, many of you disagree. It seems like you disagree because you do not like losing an argument against evolution.

  63. 63
    PaV says:

    vjt:

    I don’t plan to go through each statement point by point. I think I will make it plain that objections exist for each of these statements.

    So, e.g., the first statement:

    It’s the lincRNAs and other noncharacterized RNAs that represent the biggest problem because if all of them have a function then there will be >50,000 genes in the human genome instead of the current estimates of about 25,000 (20,000 protein-coding genes and 5,000 genes for functional RNAs). If all of those RNAs were functional they would occupy about 1% of the genome so this has has very little to do with whether 90% of our genome is junk.

    So what. The reality is that because of splicesomes and alternative sequencing, the putative 20,000 “genes” produce incredibly more numbers of actual “proteins.” If these lncRNA’s are primarily structural, then this likely has little to do with actual metabolism and development per se, but lots to do with the “machinery” of the cell, in its replication capacity. (lncRNAs are, no surprise, linked to cancer–this would be expected if they have replicational roles to play)

    The beginning of the third statement:

    As a general rule, these RNAs are longer than 200 bp and some scientists put the cutoff at 1000 bp. Simple eukaryotes, such as yeast, don’t have a lot of lncRNAs but eukaryotes with large complex genomes that are full of junk DNA seem to have a lot of different lncRNAs. The DNA regions that specify these lncRNAs are not conserved. This strongly suggests that many of the lncRNAs are spurious nonfunctional transcripts even though some of them have well-characteized functions [see On the function of lincRNAs].

    Yes, of course. And, if you look at papers on lncRNA, you find that they are so long that technologically they are hard to handle. They break up. And, of course, if they break up, and have structural roles to play, then, you will not see any function.

    To me this is somewhat hilarious because you have scientists declaring there to be “no function,” when, in fact, they’re only beginning to develop the technology to test for it. This is the complete analogue of their misplaced criticism; i.e., the scorn they pour out on us for our “God-of-the-gaps” argument (which, as we know, is not what we’re doing); meaning that once science attacks the problem, what we no attribute to “God” will turn out to have purely naturalistic causes. And here, they are proposing UNSPANNABLE GAPS! No way you can explain this “junk”! (Oh, BTW, their default position is: we’ve known that “junk-DNA” has had function for over thirty years.)

    As I wrote above: caution is in order. And, of course, the know-everything scientists will be proved wrong, and then, after an appropriate silence, they will come out and say that they knew it all along.

  64. 64
    Origenes says:

    Swamidass: Sure, a tiny number of lncRNA are functional. I said that from the beginning. All evidence suggests, however, the vast majority are NOT functional.

    Fortunately Swamidass, there is a very simple explanation for this: testing IncRNA for function is extremely difficult.
    Here researchers at the University of Bath explain why finding functions for IncRNA is so difficult:

    The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.
    In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just ‘noise’ or whether it serves any function in the cell.
    Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.

  65. 65

    So, as much fun as this is, I’m pulling out for now.

    I recall a few salient points. Even if you decided to dispute the vast majority of Biologists by claiming that the lncRNAs are usually functional, this is just a rabbit trail. It makes no difference to the evidence we have presented for CD.

    1. We have established that the match to this region includes not just this putative lncRNA, but also several other matches in the same area.

    2. These matches are of very high statistical significance, and it is very easy to verify this for yourself.

    3. Because lncRNAs are trans-acting, there is no reason for this lncRNA to be at this location in the genome. CD explains this, design (without CD) has no explanation.

    4. There is no design principle, other than wild speculation about function (bad) or common descent with design (reasonable), that explains all this data.

    I would just emphasize again, that even if this specific lncRNA is functional, the evidence strongly strongly points towards common descent. There are several other matches in this region that need to be explained, and the position of this lncRNA also needs to be explained, from a design point of view. No known design principle (other than common descent + design) explains this pattern. No one here has provided an alternative.

    Any one who cannot see this is using different rules than we use in mainstream science.

    I hope some of you take interest in biology for biology’s sake. It is not just a forum to argue about evolution.

  66. 66
    HeKS says:

    vjtorley @60

    You said:

    Remember: the onus is on us to demonstrate that most of these lincRNAs actually have a function.

    Really? Says who? And why should we accept that? This claim proceeds from the notion that non-function should be the default assumption, which proceeds from a particular paradigm that is directly informed by an a priori philosophical commitment to materialism. And yet, it is widely recognized that DNA is, for all intents and purposes, software. But in any context other than biology, the default assumption with respect to any block of software code is function, not non-function.

    Now, perhaps you would say, “But we only see clear evidence of function in a minority of the DNA code.” Great, but a stably designed piece of software would, under normal circumstances, present in exactly the same way if you were simply monitoring the execution of the compiled machine code over thousands of user sessions.

    If you were to watch the execution of machine code compiled from software engineered in a way that strictly adhered to best practice design patterns, it would not be unusual to find that 75-80% of the code never gets executed. Furthermore, if you did occasionally see little blips of execution amidst the sections that usually don’t execute at all, you likely wouldn’t notice any corresponding function in the application.

    Do you find that surprising?

    Prof. Swamidass has made a point of repeatedly talking about how counter-intuitive biology is. Well, consider this: The smarter the programmer and the more foresight he or she possesses, the greater the chance that even more of the code will never be observed to execute. Yes, a good programmer following best practices may produce software in which 80% of the code is never observed to execute, but a much better programmer may very well produce software in which much more than 80% of the code is never observed to execute. And the lack of any execution of this vast majority of code is actually the desired outcome, even though it is entirely functional and purposeful. How is that for counter-intuitive? People need to understand that “counter-intuitive” is not the same thing as “illogical” or “nonsensical”. It often just means that the guiding logic encompasses more factors than one might initially expect.

    But if this is the state of affairs we observe in our own intelligently designed software projects, and if all manner of qualified people working in both software design and, shall we say, DNA design (and biochemistry, etc.) readily acknowledge that DNA is software and uses the same types of design patterns that humans use in software design, why do we suddenly abandon the remarkable connection between software and DNA by assuming non-function for unexecuted DNA when, in the exact same situations and under the exact same circumstances, we would consistently assume function for unexecuted software code?

    The only readily available answer to this question seems to be that biologists, stumbling along under the intellectual constraints of Methodological Naturalism, simply assume that DNA is not the product of intelligent design. But if we find their guiding philosophical assumptions to be unconvincing and unnecessary, why should we join them in their otherwise absurd assumption that any block of DNA for which we don’t currently know of any function must therefore be functionless? Given the context, how is this anything other than a blatant argument from ignorance? And to the extent that arguments for Universal Common Descent (UCD) are based on assumptions of shared non-function, how does UCD itself not constitute an hypothesis based mostly on arguments from ignorance? If it ultimately turned out that all or substantially all of DNA was functional, how do you think that would impact the case for UCD?

    Take care,
    HeKS

  67. 67
    bornagain77 says:

    Of related interest, here is a study that came out of Dr junk DNA Moran’s own backyard, i.e. The University of Toronto

    Shedding light on the ‘dark matter’ of the genome – May 19, 2016 – Source: University of Toronto
    Excerpt: What used to be dismissed by many as “junk DNA” is back with a vengeance as growing data points to the importance of non-coding RNAs (ncRNAs) — genome’s messages that do not code for proteins — in development and disease.,,
    ncRNAs come in multiple flavours: there’s rRNA, tRNA, snRNA, snoRNA, piRNA, miRNA, and lncRNA, to name a few, where prefixes reflect the RNA’s place in the cell or some aspect of its function. But the truth is that no one really knows the extent to which these ncRNAs control what goes on in the cell, nor how they do this. The new technology developed by Blencowe’s group has been able to pick up new interactions involving all classes of RNAs and has already revealed some unexpected findings.
    https://www.sciencedaily.com/releases/2016/05/160519120935.htm

    Bet that didn’t go down well in the faculty lounge at the University of Toronto 🙂

  68. 68
    bill cole says:

    From a paper published today on snoRNA’s role in alternative splicing.

    Using RNA sequencing and molecular biology techniques, the researchers found that often snoRNAs not only modify ribosomes, but actually perform a dual function: they can also regulate alternative splicing, resulting in regulating the alternative inclusion of small pieces in proteins, which regulates protein function, thus inhibiting the generation of wrong protein variants.

    These new functions can explain the role of snoRNAs in human diseases, as upon their loss the formation of wrong protein variants can no longer be prevented.

    In mechanistic studies, the researchers also showed that short synthetic RNAs could be used as a substitute for the missing snoRNAs. This could point to a possible therapy for genetic hyperphagia (a condition that causes extreme hunger or appetite) and some forms of cancer.

    “This research helps us to understand the unexpected dual role of snoRNAs in gene regulation. It further points to the important role played by small non-coding RNAs in alternative splicing, which is a major contributor to the diversity of the human proteome, and defects in which result in numerous diseases including cancer. With further research in this area we may be able to design new therapies against human diseases,” said Prof. Ruth Sperling from the Department of Genetics at the Hebrew University’s Alexander Silberman Institute of Life Sciences.

  69. 69
    Querius says:

    Well, the forum is called Uncommon Descent. 😉

    First off, let me express my gratitude for the time and thought that went into these posts. Yes, I read them all. I’d also add my appreciation for those posted by bornagain77, which are enlightening and contain interesting links.

    From a macro perspective, we observe amazing types of life that demonstrate astonishing adaptability and variety. Looking deeper, we observe astonishing cellular complexity far beyond our original assumption of “protoplasm.” Deeper still, we discover a plethora of astonishing chemical cycles, and then at the level of analysis of DNA, we find . . . 99% junk with no purpose. Really?

    Based on observation, it’s far more likely that we’re 99% ignorant, not to mention arrogant.

    HeKS described compiled computer code, which far simpler by comparison to what we understand about how DNA is expressed, noting that no competent programmer would rip out code simply based on whether it’s observed to be executed (error trapping code is rarely executed). And yet we assume that genetic code must be junk.

    The big problem with common descent is that it’s lacking a credible mechanism to drive it to greater complexity and new body plans. Random recombination won’t generate a Tesla in a trash heap no matter how long or hard you shake it.

    So here’s a challenge, Professor Swamidass. Take a strain of non-motile bacteria and put them in an environment favoring motility. Subject the samples to high levels of ionizing radiation to simulate the passage of deep time over many generations of bacteria. It should be easy then to demonstrate common descent from the results of these bacteria evolving cilia, flagella, legs, and maybe even propellers or rocket engines!

    Otherwise, it’s all just a thumb suck—philosophy, not science.

    -Q

  70. 70
    PaV says:

    Prof. Swamidass:

    You wrote, challengingly:

    1. We have established that the match to this region includes not just this putative lncRNA, but also several other matches in the same area.

    2. These matches are of very high statistical significance, and it is very easy to verify this for yourself.

    3. Because lncRNAs are trans-acting, there is no reason for this lncRNA to be at this location in the genome. CD explains this, design (without CD) has no explanation.

    4. There is no design principle, other than wild speculation about function (bad) or common descent with design (reasonable), that explains all this data.

    Your #4 is my position; but, I don’t consider “common descent with design” to any longer be what is commonly called “common descent.” I call it “common ancestry.” There is too much commonality to think that everything is “de novo”. However, OTOH, as in the case of the bird feather (still no comment by you), common descent is a non-starter as an explanation. So, I’ll stick with “common ancestry.”

    BTW, we always enjoy it when authors visit the site and discuss things. It’s always a learning experience.

  71. 71
    Eric Anderson says:

    Clavdivs @57:

    Haven’t scientists discovered that junk DNA has virtually zero fitness cost for large organisms?

    Why in the world would someone say that?

    Are you saying that having junk DNA has no fitness cost, that not having junk DNA has no fitness cost, or that junk DNA has no function? None of these, particularly the latter two, are even close to accurate.

  72. 72
    CLAVDIVS says:

    Eric Anderson @ 71

    Dr JDD claimed puzzlement at how evolution can build complex things like eyes and giraffes, but cannot get rid of a bit of junk DNA.

    My point was that a little bit of genuinely non-functional DNA has virtually no cost to a large organism, so there is no selective pressure to remove it … it doesn’t really hurt to have it.

    On the other hand, in a species with eyes, for example, an individual without eyes has a huge disadvantage, so there is selective pressure to maintain eyes.

    So it should be no surprise that whilst evolution is claimed to build eyes and giraffes, it is not always expected to get rid of a bit of junk DNA.

  73. 73
    CLAVDIVS says:

    Origines @ 59

    Not having “junk DNA” would have an enormous fitness cost.

    I said having junk DNA would have virtually no fitness cost.

    Tell that to bacteria.

    I said “for large organisms”.

    Natural selection explains what is not, not what is.

    We’re talking about “evolution” not just natural selection.

  74. 74
    bornagain77 says:

    It is amazing to me to see Christians who profess to believe that God created, and sustains, the universe and all life in it can be so easily persuaded that perhaps God took a chimp-like creature and morphed it into a human instead of creating humans separately.

    IMHO, The evidence for common ancestry is based on ignorance, on undisciplined imagination, and is severely overblown, especially when compared to the actual physical evidence from the fossil record against the hypothesis of common ancestry. The overall pattern of evidence in the fossil record, by itself, certainly does not support the ‘God morphed a Chimp into a Human’ scenario. To reiterate, the Cambrian explosion, and the fossil record in general, reveal an undeniable pattern of ‘top down’ sudden appearance, and certainly does NOT reveal a pattern of God gradually morphing one creature into another creature in a ‘bottom up’ fashion. The only place one encounters any real stiff resistance to this fact that the fossil record is completely antagonistic to Darwinian claims is with the human fossil record itself. Here, besides the many fraudulent fossils that Darwinists have proffered over the last century, fossils contending to be the missing link between apes and humans are a dime a dozen. Each contender has been shot down when cooler heads prevail over the media hype. Yet, despite the media hype on fossils purporting to be ‘the missing link’, and the fraudulent cartoon drawings showing a chimp morphing into a human, (one fraudulent drawing of which Torley displayed on his other post), the missing link between humans/neanderthals and apes is still missing.

    “We have all seen the canonical parade of apes, each one becoming more human. We know that, as a depiction of evolution, this line-up is tosh (i.e. nonsense). Yet we cling to it. Ideas of what human evolution ought to have been like still colour our debates.”
    Henry Gee, editor of Nature (478, 6 October 2011, page 34, doi:10.1038/478034a),

    Paleoanthropologist Exposes Shoddiness of “Early Man” Research – Feb. 6, 2013
    Excerpt: The unilineal depiction of human evolution popularized by the familiar iconography of an evolutionary ‘march to modern man’ has been proven wrong for more than 60 years. However, the cartoon continues to provide a popular straw man for scientists, writers and editors alike.
    ,,, archaic species concepts and an inadequate fossil record continue to obscure the origins of our genus.
    http://crev.info/2013/02/paleo.....hoddiness/

    New York Times Inherits the Spin, Republishes Darwinists’ Error-Filled “Answers” to Jonathan Wells’ – 2008
    Excerpt: And all three of these textbooks include fanciful drawings of ape-like humans that help to convince students we are no exception to the rule of purposelessness.
    Some biology textbooks use other kinds of illustrations ,,,
    http://www.evolutionnews.org/2.....10581.html

    “A number of hominid crania are known from sites in eastern and southern Africa in the 400- to 200-thousand-year range, but none of them looks like a close antecedent of the anatomically distinctive Homo sapiens…Even allowing for the poor record we have of our close extinct kin, Homo sapiens appears as distinctive and unprecedented…there is certainly no evidence to support the notion that we gradually became who we inherently are over an extended period, in either the physical or the intellectual sense.”
    Dr. Ian Tattersall: – paleoanthropologist – emeritus curator of the American Museum of Natural History – (Masters of the Planet, 2012)

    Man is indeed as unique, as different from all other animals, as had been traditionally claimed by theologians and philosophers.
    Evolutionist Ernst Mayr (What Evolution Is. 2001)

    Human Origins and the Fossil Record: What Does the Evidence Say? – Casey Luskin – July 2012
    Excerpt: Indeed, far from supplying “a nice clean example” of “gradualistic evolutionary change,” the record reveals a dramatic discontinuity between ape-like and human-like fossils. Human-like fossils appear abruptly in the record, without clear evolutionary precursors, making the case for human evolution based on fossils highly speculative.
    http://www.evolutionnews.org/2.....61771.html

    Later Hominins: The Australopithecine Gap – Casey Luskin – August 2012
    Excerpt: Paleoanthropologist Leslie Aiello, who served as head of the anthropology department at University College London, states that when it comes to locomotion, “australopithecines are like apes, and the Homo group are like humans. Something major occurred when Homo evolved, and it wasn’t just in the brain.” The “something major” that occurred was the abrupt appearance of the human body plan — without direct evolutionary precursors in the fossil record.
    http://www.evolutionnews.org/2.....62891.html

    Skull “Rewrites” Story of Human Evolution — Again – Casey Luskin – October 22, 2013
    Excerpt: “There is a big gap in the fossil record,” Zollikofer told NBC News. “I would put a question mark there. Of course it would be nice to say this was the last common ancestor of Neanderthals and us, but we simply don’t know.” –
    http://www.evolutionnews.org/2.....78221.html

    Moreover, the morphological, anatomical, and genetic dissimilarities between chimps and humans are far more pronounced than Darwinists and Theistic evolutionists are, apparently, ever willing to admit to.

    A Closer Look At Human and Chimp Similarities and Differences – video (2016)
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1134643976548534/?type=2&theater

  75. 75
    Origenes says:

    CLAVDIVS,

    Dr JDD: I always find it supremely hilarious how evolution can account for a complex eye multiple independent times by random chance (convergence), can (just because food decides to grow higher) account for an incredible complex animal such as the giraffe with such distinct needs, but cannot get rid of a bit of junk DNA and stop it from being transcribed once it is broken (yet avoid somehow its translation).

    Indeed, how can evolution operate with jaw dropping precision and, at the same time, be so incompetent — not being able to get rid of a bit of junk DNA? The awe-inspiring capability to build an eye or a giraffe, seems to imply abilities like getting rid of bits of junk DNA.

    In order to resolve this dichotomy, one has to explain: (1) where the extreme precision building capability comes from, (2) where the incompetence comes from and (3) how the two are reconcilable.

    Your attempts at (1) are, as far as I can see, : “… features like eyes or necks where, if favoured by the environment, not having them has a big fitness cost.” and “there is selective pressure to maintain eyes”. Attempts, which, as I have argued (see #59), are grossly insufficient.

  76. 76
    CLAVDIVS says:

    aap @ 58

    It is not surprising that those who have been fed and watered at the evolution trough through the public education systems are going to believe that the church is out of step with the rest of the world, just as they think that much of the church is out of step with the world on many other social issues, which of course the church should be.

    If that’s how you think the church should be – withering away because it is out of step with the scientific world – then there’s no problem, because that’s what’s happening.

    Just don’t try to pretend later that nobody warned you …

  77. 77
    mw says:

    Consider the opossum: the evidence for common descent.

    When I consider looking at a possum, I think, ‘design a possum based on evolutionism.’ Then, describe, by evolutionism, or more to the point, imagine, how such an animal, indeed any life form, came to be, using the parameters of Darwinism in general.

    The secondary thought came, you can describe ‘exactly,’ give or take some fancy footwork, how any life form came into existence, every time. The system of thought is akin to belief in infallibility.

    Surely therefore, that is why the theory is largely faith based, and more to the point; because we cannot evolve a possum – ever – by experimental means or any other means.

  78. 78
    CLAVDIVS says:

    Origines @ 75

    … how can evolution operate with jaw dropping precision and, at the same time, be so incompetent — not being able to get rid of a bit of junk DNA? …
    In order to resolve this dichotomy, one has to explain: (1) where the extreme precision building capability comes from, (2) where the incompetence comes from and (3) how the two are reconcilable.

    If we grant (1) to evolutionists – that evolution has precision building ability – then (2) and (3) are easily explained and neither contradictory nor absurd.

    To repeat … The reason evolution may not remove functionless DNA is not incompetence but merely indifference. A trait that has virtually no effect on fitness is invisible to selection and there is no particular reason for evolution either to remove it or to maintain it. It is therefore absolutely no surprise, according to mainstream biology, that functionless DNA may hang around in the genome.

    On the other hand, traits that are under strong selection – like vertebrate eyes – tend strongly to be maintained. Variations that reduce function are ruthlessly eliminated, so the tendency is to accumulate only beneficial variations, thus gradually increasing in complexity.

    If you want to argue that evolution doesn’t work at all (deny (1)) then, sorry, that’s just a completely different point than the one I was discussing with JDD.

  79. 79
    Andre says:

    Why would eyes be under strong selection? When there was no eyes how did natural selection come to the realization…..

    “We need eyes!”

    How does a random, purposeless and unintelligent process do that?

    I wonder……

    Seems to me that people like CLAVDIVS have still not realized that Darwinian evolution can only work with what it has, it holds no power over anything it does not, even Darwin knew that.

  80. 80
    CLAVDIVS says:

    mw @ 77

    I live in the land of Oz, and I have found and examined many marsupial skulls such as those of possums, kangaroos, wallabies, marsupial mice and even wombats.

    Their similarities are quite obvious compared to the skulls of placental mammals like dogs and cows.

    In simple terms, we know from our own family trees that the closer the relationship, the closer the similarities. We also know from genetic science that patterns of similarities and differences in DNA can be used to establish relatedness in courts if law.

    Therefore, even if you believe in common design, the logical conclusion is that marsupials are more closely related to each other than to other mammals, which implies a more recent common ancestor for all the marsupials, and a more distant common ancestor for all mammals.

    If your alternative explanation is the ex nihilo creation of lifeforms with no common ancestry, then I refer you to my post @ 56 about how young people are leaving the church in droves because of the perception that Christianity is anti-science.

  81. 81
    Andre says:

    CLAVDIVS….

    Common descent is an assumption not a fact. Every real science paper you will ever open on cladistics says that.

    It is an assumption not a fact!

  82. 82
    CLAVDIVS says:

    Andre @ 79

    Eyes being under strong selection is a bit like money – once you start earning more, you start to depend on it and it becomes difficult to go backwards.

    Arguing about where eyes come from in the first place is irrelevant to JDD’s point that I was responding to – namely, that there is something absurd about evolution claiming to be able to build complex eyes, but being unable to remove a little bit of useless DNA. The explanation is simple: eyes are under strong selection pressure, but useless DNA is under virtually no selection pressure.

  83. 83
    CLAVDIVS says:

    Andre @ 81

    If you want to describe everything that is not proven with 100% certainty as an “assumption”, that’s fine.

    That’s not the way reasonable people use the word “assumption” when talking about scientific ideas. Nothing in science is 100% proven aside from the axioms of logic, so by your terminology every scientific idea is an “assumption”, no matter how rigorously supported and universally accepted.

    And that’s just silly.

  84. 84
    bornagain77 says:

    Darwinian evolution is certainly not rigorously supported. In fact, Darwinian evolution is a unfalsifiable pseudo-science. No matter what finding, even completely contradictory findings, the findings are always crammed into the Darwinian narrative no matter how contrary they are to the core theory:

    “Being an evolutionist means there is no bad news. If new species appear abruptly in the fossil record, that just means evolution operates in spurts. If species then persist for eons with little modification, that just means evolution takes long breaks. If clever mechanisms are discovered in biology, that just means evolution is smarter than we imagined. If strikingly similar designs are found in distant species, that just means evolution repeats itself. If significant differences are found in allied species, that just means evolution sometimes introduces new designs rapidly. If no likely mechanism can be found for the large-scale change evolution requires, that just means evolution is mysterious. If adaptation responds to environmental signals, that just means evolution has more foresight than was thought. If major predictions of evolution are found to be false, that just means evolution is more complex than we thought.”
    ~ Cornelius Hunter
    http://www.uncommondescent.com.....ent-609503

    i.e. Despite the false bravado of Darwinists that CD is well supported, the fact of the matter is that the evidence consistently runs contrary to the hypothesis of UCD. Moreover, nothing is ever allowed to challenge the core theoretical assumptions of Darwinian evolution and thus Darwinian evolution is, by all rights of science, an unfalsifiable pseudo-science.

  85. 85
    bornagain77 says:

    Torley, since you are a James Tour fan, and have written on him quite a bit, I think you may appreciate this article he wrote:

    Animadversions of a Synthetic Chemist – James Tour – May 19, 2016
    Excerpt: The world’s best synthetic chemists, biochemists, and evolutionary biologists have combined forces to form a team — a dream team in two quite distinct senses of the word. Money is no object. They have at their disposal the most advanced analytical facilities, the complete scientific literature, synthetic and natural coupling agents, and all the reagents their hearts might desire. Carbohydrates, lipids, amino acids, and nucleic acids are stored in their laboratories in a state of 100% enantiomeric purity.
    Would the dream team — please — assemble a living system?
    Take your time, folks, take a few billion years.
    Nothing? Well, well, well.
    Let us assume that all the building blocks of life, and not just their precursors, have been made to a high degrees of purity, including homochirality where applicable — the carbohydrates, the amino acids, the nucleic acids, and the lipids. They are stored in cool caves, away from sunlight, and away from oxygen. These molecules are indifferent to environmental degradation.
    And let us further assume that they are all stored in one comfortable corner of the earth, not separated by thousands of kilometers or on different planets.
    And that they all exist not just in the same square kilometer, but in neighboring pools where they can conveniently and somehow selectively mix with each other as needed.
    Now what? How does the dream team assemble them without enzymes?
    Very well. Give the dream team polymerized forms: polypeptides, all the enzymes they desire, the polysaccharides, DNA and RNA in any sequence, cleanly assembled.
    Ready now?
    Apparently not. ,,
    Those who think scientists understand the issues of prebiotic chemistry are wholly misinformed. Nobody understands them. Maybe one day we will. But that day is far from today. It would be far more helpful (and hopeful) to expose students to the massive gaps in our understanding. They may find a firmer — and possibly a radically different — scientific theory.
    The basis upon which we as scientists are relying is so shaky that we must openly state the situation for what it is: it is a mystery.
    http://inference-review.com/ar.....ic-chemist

  86. 86
    Eric Anderson says:

    gpuccio @1:

    Frankly, I am amazed at the obstinacy with which many people in the ID field stick to denial of the evidence for common descent.

    Yeah, but let’s remember that your version of “common descent” is not the same as the “common descent” being pushed by the materialist evolutionary narrative. When we get you to clearly articulate your proposal 🙂 I’m confident most ID proponents would be just fine with your idea, at least in principle, as a potential avenue of intelligent design.

    What isn’t impressive are the various comparative observations and, in many cases, cherry-picked examples that are used as a hammer to hit people over the head and loudly proclaim the truth of the RM+NS=Everything doctrine.

    No doubt there are some who refuse to consider any kind of continuity between species over time due to some religious dogma. In my experience, those individuals are very few and far between. If we listen carefully to people’s concerns about the traditional materialistic common descent propaganda, including many of the concerns expressed on this thread, we find that the concerns are much more nuanced and thoughtful than simply a refusal to accept continuity over time.

  87. 87
    Phinehas says:

    Prof S:

    If they think it is functional, ask them why, and how they would demonstrate it.

    What about if they think it is non-functional? Can I still ask them why, and how they would demonstrate it? I think HeKS has demonstrated quite clearly why the burden of proof should not be shifted as you are doing.

    If you still persist in disagreeing with biologists, the onus is on you. Frankly, you will probably need to go get a PhD, start a lab, get some grants, and come back to me after 10 years of dedicated scientific work to convince us on this point. If you were successful, you might even become famous. Of course, none of you are going to do that, because most of you could care less how lncRNAs function, other than to use them as a rhetorical club against evolution.

    You seem to have fallen into a habit of posting things like the above. You should know that they do not paint you in a very good light. This does not discredit your argument, but the above credits neither you nor your argument.

  88. 88
    Andre says:

    CLAVDIVS.

    Creature A has no eyes it then under strong selection via a random purposeless process have eyes emerge…. You think that is reasonable? Are you truly being reasonable in your promotion of such twaddle? I don’t think you really believe that….

  89. 89
    Andre says:

    Eric

    Thank you for articulating it so well. You are on point. Mung mentioned the other day that even young earth creationists are fine with common descent.

  90. 90
    wd400 says:

    Are you saying that having junk DNA has no fitness cost, that not having junk DNA has no fitness cost, or that junk DNA has no function? None of these, particularly the latter two, are even close to accurate.

    All these statements are true (at least for Eukaryotes in small populations), the last one by definition.

  91. 91
    bill cole says:

    Eric@86

    Yeah, but let’s remember that your version of “common descent” is not the same as the “common descent” being pushed by the materialist evolutionary narrative. When we get you to clearly articulate your proposal 🙂 I’m confident most ID proponents would be just fine with your idea, at least in principle, as a potential avenue of intelligent design.

    This is exactly right so common decent is mis leading. What were are observing is common biochemistry. Common decent implies that we decended from natural cause but if you look at these transitions we have no idea what mechanisms could have caused this in nature. Including gene timing and splicing the biochemical differences between man and apes is enormous.

  92. 92
    Origenes says:

    CLAVDIVS:

    Origenes: … how can evolution operate with jaw dropping precision and, at the same time, be so incompetent — not being able to get rid of a bit of junk DNA? …
    In order to resolve this dichotomy, one has to explain: (1) where the extreme precision building capability comes from, (2) where the incompetence comes from and (3) how the two are reconcilable.

    If we grant (1) to evolutionists – that evolution has precision building ability – then (2) and (3) are easily explained and neither contradictory nor absurd.

    This doesn’t make sense to me.

    The question raised is: how can it be coherently claimed, that evolution has jaw dropping precision building ability, considering its inability to get rid of chunks of junk DNA. Which is somewhat akin to the question: how can anyone, who is unable to tie his own shoes, be expected to be able to survive alone in the Amazone rainforest?
    Your reply boils down to: the riddle is solved by assuming that he can survive the Amazone rainforest.

  93. 93
    aap says:

    Clavdivs at 76
    Don’t worry about the Church of JESUS CHRIST, it is doing well in most parts of the world with the exception of the west, where it is in severe decline. The mainline churches in Europe that adopted theistic evolution into their theology a few generations ago are all on the ropes, ready to be tossed out of the ring. As JESUS said: “Salt that has lost its saltiness is no longer good for anything except to be thrown out and trampled by men.” Matthew 5:13. The churches in Europe are in for a good and well deserved trampling. The mainline churches in North America are following the same false theology and the same path to irrelevance. When the church adopts the philosophies of the world it ceases to be the Church of JESUS CHRIST and will be spewed out of His mouth. It is the Pentecostal and Evangelical Biblical churches that still believe in CHRIST and His Word that are growing in many parts of our world. Creation ministries are expanding everywhere. The Name and Word of CHRIST is being lifted up to all nations and many are coming into the Kingdom. To GOD be the glory!

  94. 94
    mw says:

    Thanks CLAVDIVS for the link @ 56.

    Alas, I am well aware of such things. In Britain, where I live, the end of Christianity for being significant, is 2067. That is projected from the last two national censuses.

    You cite, as the reason for loss of faith; belief in divine law is anti-science.

    Well; as such science so-called ever evolved an opossum from a non opossum. And before that, a none opossum, from dead, lifeless, sterile dust?

    Prove an opossum evolved, or anything else that matter by experimental means (I do not mean evolve within the limits of the opossums kind). Check that out for any life form!

    One reason for such a decline in the Judaeo-Christian faith, is because of the apparent slight of hand of Darwinism, intended or not; its iron curtain type of mentality, which largely fails to point out the flaws in the Darwinian system. Afraid that such a powerful system of thought, cannot and surely must not be wrong; not wanting to repeat and use honest words in abundance. Afraid a surge of voices is gaining notice, that no solid proof exists for the theory for it to be given the gold standard: a true scientific law.

    Christianity can never be against true science. See, http://kolbecenter.org/more-scientific/

    However, the the loss of faith is also as a result of Christians having a hand in the spiritual sickness; certainly the Pontifical Academy of “evolutionism.”

    As a Catholic, I am just waiting for a Pope to declare Darwinism true!

    As for the poor state of the health of the faith, it is matched by the increasing poor health of Darwinism.

    Still, I believe, divine law must have divine backing: therefore, an upsurge is inevitable; built on Sinai, which is the central point of the Sabbath; to remember the Creation Miraculous, which Jesus also fulfilled.

    Of course, Jesus is not scientific, you may say. Nevertheless, as witnessed, and no doubt reported just as accurately as any scientific observation; convinced what had been witnessed as unbelievable by natural standards; that Yahweh/Jesus/God, willed/spoke/breathd, and life reformed in various ways, matter obeyed and food increased. One could go on and on.

    Jesus proved Master of Biology, bringing life back into lifeless Lazerus, and in Himself as He said He would.

    What your example appears to also prove, is that the belief in miracles no longer prevails. That is correctable, as there is ample evidence of miracles.

    I believe, time and Divine intervention will have their day, no matter how bad things seem.

  95. 95
    Dionisio says:

    The several lncRNA “experts” commenting in this discussion thread might enjoy reading carefully the papers referenced in the following links:

    http://www.uncommondescent.com.....ent-609668

    http://www.uncommondescent.com.....ent-609671

  96. 96
    Dionisio says:

    To Whom This May Concern:
    There are several (at this point 8) lncRNA-related papers referenced in the comments #1639-1646 posted in the thread pointed to by the following link:

    http://www.uncommondescent.com.....ent-609729

    Please, note that all those papers – taken together- seem to state that we ain’t seen nothing yet. 🙂

  97. 97
    Dionisio says:

    Please, note that either way (CD or UD) is fine, as long as it is clearly described with all details. Did anyone get that detailed description yet? 🙂

  98. 98
    Dionisio says:

    gpuccio @1

    “…all the new complex information which arises in all species is designed, and cannot be explained by any neo-darwinian theory, or more generally by any non design theory which does not imply the explicit intervention, in time and space, of some conscious, intelligent and purposeful being as a designer. Not even a single new complex protein can be explained without a designer.”

    Agree.

    I’ve not quite understood the ongoing “CD vs. UD” discussion, but have left it on the shelf, while focusing on the current research about the known complex specified information processes seen within the biological systems, feedback and feed forward loops in regulatory networks, etc. That’s my main interest in biology. Systems Biology courses by Prof. Uri Alon at the Weizmann Institute and Prof. Jeff Gore at MIT are very interesting.
    However, since the lncRNA subject has popped up here and you have commented in this thread, I would like to ask you how do the lncRNAs relate to the CD vs. UD discussion?
    Also, can we say that most lncRNA are nonfunctional? See my posts @95-97.
    Thank you.

  99. 99
    Mung says:

    bill cole @21:

    The beef is that without a mechanism it is bad science.

    You had parents. Your parents had parents. Their parents had parents. There is no missing mechanism.

    I repeat, even the most ardent young earth creationist accepts common descent. They accept that there exists some mechanism capable of explaining both descent from ancestors on the ark and divergence from those ancestors into the species we have at present. So where’s the beef?

  100. 100
    Mung says:

    Andre: You do know that common descent is just an assumption right?

    As a young earth creationist, how would you argue for the common descent from the animals on the ark?

  101. 101
    Mung says:

    Andre: 1.a thing that is accepted as true or as certain to happen, without proof

    So the lack of common descent is an assumption, and young earth creationists accept the assumption of the lack of common descent, except when they do not accept the assumption of the lack of common descent. How do they distinguish?

    Or do they accept the assumption that each modern species was specially created last Thursday?

  102. 102
    Mung says:

    Prof. S. Joshua Swamidass:

    Once again, if we reject common descent, why do we have this broken gene? What design principle explains this pattern?

    Who the hell rejects common descent? Even the most ardent young earth creationist accepts common descent. What will it take to get this simple fact through your thick skull?

  103. 103
    HeKS says:

    Mung @99

    I’m not a YEC, but I agree that Common Descent, in the sense of continuous descent, from one generation to the next, through a reproductive process, is probably unproblematic in many cases, such as in any instance that involves the degradation of a more robust genome, where diversity arises primarily through the loss or breakage of previously functional code. Conceivably, this could happen very quickly, with diversity arising very quickly after some organism arrives on the scene, followed by ongoing stasis resulting from the the original genetic potential being exhausted.

    Where I think Common Descent, in the sense described above, becomes problematic, is where diversity or disparity arises through any significant influx of new information. In those cases, even if it turned out that the designer(s) appropriated the material of some preexistent organism and modified it, it starts to become problematic to refer to the new organism as being a product of “Common Descent”, since whatever would define it as the new organism it is would have arisen not as a result of the passing on of genetic contents through the reproductive process but by means of a purposeful infusion of new information from some external source.

    And who knows if the organism would even have been alive at all points during such a process? At what point would we say that an organism produced in such a fashion was actually a new “creation” of some sort and that describing it as a product of “Common Descent” was more misleading than helpful?

    Take care,
    HeKS

  104. 104
    CLAVDIVS says:

    aap @ 93

    Actually the fastest growing ‘religions’ in the world over the past 100 years are atheism, agnosticism and spiritualism. Christianity is losing ground.

    Not only that, the regions where Christianity is still growing – Africa, South America and Asia – are those where there is little perceived conflict between Christianity and science. Christianity is weakening in North America and Europe, where the conflict is much more perceptible. And Christianity is weakest of all in the muslim world, where creationism is the most dominant view of origins.

  105. 105
    Dionisio says:

    #95-98 addendum:
    here’s a comment on lncRNA found in this 3yo paper:

    “Despite general agreement that some long noncoding RNAs are functional and others are not, opinions vary widely as to the fraction that is functional (Kowalczyk et al., 2012). Because of their marginal sequence conservation and a sense that spurious transcripts would impose minimal fitness cost, we suspect that most are not functional. However, even a scenario in which only 10% are functional implies the existence of more than a thousand human loci generating noncoding transcripts with biological roles. These enigmatic RNAs will consume decades of effort for many labs undertaking molecular, mechanistic, and phenotypic analyses. And regardless of function, long noncoding RNAs might have diagnostic applications, with changes in their expression already associated with cancer and several neurological disorders (Prensner et al., 2011; Brunner et al., 2012; Ziats and Rennert, 2013).”

    lincRNAs: Genomics, Evolution, and Mechanisms
    Igor Ulitsky and David P. Bartel
    DOI: http://dx.doi.org/10.1016/j.cell.2013.06.020

  106. 106
    CLAVDIVS says:

    Because of their marginal sequence conservation and a sense that spurious transcripts would impose minimal fitness cost, we suspect that most are not functional.

    Exactly what I’ve been saying all along.

  107. 107
    mw says:

    Hi CLAVDIVS @ 104:
    ——————–
    ‘Actually the fastest growing ‘religions’ in the world over the past 100 years are atheism, agnosticism and spiritualism. Christianity is losing ground.’
    ——————–

    Well, I am surprised you place atheism in the same category as witchcraft, as may be held to be is “spiritualism,” a meaning which is: “a system of belief or religious practice based on supposed communication with the spirits of the dead, especially through mediums.”

    Such is forbidden in Judaeo-Christian scripture, declared so by Yahweh.

    Following that, you claim “atheism” is among such “religions”!

    You declare your preferred statistics as confirmation of the emptiness of such scripture.

    Come, come, surely you can do better than that, when the same historic scripture, expertly recorded by truthful witnesses, declares that such appears a regular occurrence with fallen humans!

    Clearly you dismiss such historic statistics.

    Still, nation moving miracles happen, and will do again; based on historic evidence. Happy days.

  108. 108
    bill cole says:

    Mung@99

    You had parents. Your parents had parents. Their parents had parents. There is no missing mechanism.

    I repeat, even the most ardent young earth creationist accepts common descent. They accept that there exists some mechanism capable of explaining both descent from ancestors on the ark and divergence from those ancestors into the species we have at present. So where’s the beef?

    If you are saying common decent limits us from kinds derived from the ark then I agree. It is when two different kinds are created from a common ancestor solely through reproduction that I think we have inconsistency from what we know about biochemistry. Kinds were not designed to diverge. I do not think a new functional genome with different splicing sequences can emerge through reproduction. This theory has to much counter evidence too be viable. The theory as it stands is misleading because it does not imply inheritance from the ark. It implies that chimps and man split from a common ancestor 6 million years ago. Now that we can observe the biochemical differences there is no way to reconcile this idea. I do not have a theological problem with common decent I simply think it is terrible science given the current evidence.

  109. 109
    CLAVDIVS says:

    Hi mw @ 107

    Well, I am surprised you place atheism in the same category as witchcraft …

    I put ‘religion’ in quotes to signify a unorthodox usage of the word, because I’m really not interested in this sort of nitpicking.

    You declare your preferred statistics as confirmation of the emptiness of such scripture.
    Come, come, surely you can do better than that..

    What you pretend to smear as merely “my preferred statistics” are in fact from the World Religion Database, the leading scholarly source of global religious demographic data, researched at Boston University, edited by professional demographers, and published by Brill, a renowned international academic publisher established in The Netherlands in 1683.

    Also, I made no claim about the “emptiness of scripture” and have not “dismissed historic statistics” so stop trying to put words in my mouth.

    … the same historic scripture, expertly recorded by truthful witnesses, declares that such appears a regular occurrence with fallen humans!

    Declares that what appears a regular occurrence? I don’t know what you’re talking about.

    Oh.

    And you haven’t responded to my point that the evidence shows that wherever creationism grows strong, Christianity grows weak.

  110. 110
    mw says:

    Hi CLAVDIVS @ 109:

    ————
    “And you haven’t responded to my point that the evidence shows that wherever creationism grows strong, Christianity grows weak.”
    ————

    Well, start from Sinai, where a developing nation grew from a creationist God, and remembered every Sabbath.

    Happy days indeed, when the miraculous was witnessed over forty years, daily, by a developing nation.

    Clearly, not knowingly wanting to put words in your mouth. Jesus/God of Sinai was weak, or is that humans?

  111. 111
    mw says:

    PS CLAVDIVS:

    ———————
    ‘What you pretend to smear as merely “my preferred statistics” are in fact from the World Religion Database, the leading scholarly source of global religious demographic data, researched at Boston University, edited by professional demographers, and published by Brill, a renowned international academic publisher established in The Netherlands in 1683.’
    ———————–

    Very impressive CLAVDIVS.

    “Smear,” come come. You do my faith an ‘injustice,’ not wanting to put words in your mouth. A little lively banter.

    However, with respect, the statistics from the Judaeo-Christian Scripture’s are equally as valid as your ‘prefarred’ stats; again, not wishing to put words in your mouth. Humans prefer themselves as God, and fall away if left without divine intervention within the limits of free will.

  112. 112
    ThickPython says:

    @74, bornagain77:

    A Closer Look At Human and Chimp Similarities and Differences – video (2016)
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1134643976548534/?type=2&theater

    Hi BA,

    I’m assuming that video is yours, yeah?

    Just wanted to point you towards two of my blog posts that directly address the Tomkins paper that you mention towards to end of that video:

    1. https://roohif.wordpress.com/2016/03/22/is-1-a-myth/

    This one addresses his most recent human/chimpanzee comparison paper in which he gets an overall result of 88%.

    2. https://roohif.wordpress.com/2015/10/19/how-big-is-the-chimpanzee-genome/

    This addresses his claim that the chimpanzee genome is 8% larger than the human genome.

    I haven’t fully addressed his “Genetic gap widens between humans and chimps” article, but the research I have done so far is pretty damning.

    In short, Tomkins is a hack.

  113. 113
    bornagain77 says:

    Sorry Python, you’ve insulted my posts as “Gish Gallop”, thus I respond in kind and will ignore your pointless “troll tripe” as well (free will allows me to do such things you see 🙂 ). I got much better things to do than arguing with a Darwinian dogmatist, such as watching this recent upload on Robert Marks’s youtube channel:

    Can We Create Minds From Machines? Erik J. Larson, PhD
    Presented on the campus of Baylor University
    May 18, 2016
    https://www.youtube.com/watch?v=vw8SVybnOGY

  114. 114
    HeKS says:

    Hi ThickPython,

    I read your linked article on the 1% myth issue. As for your own finding of between 97-99% similarity, is that in a comparison of protein coding regions or across the entire genome, including what you may think is junk?

    Take care,
    HeKS

  115. 115
    Eric Anderson says:

    HeKS @114:

    ThickPython, a couple of other questions, if you don’t mind:

    Is the 97-99% similarity comparison done on a linear basis across the entire genome (or at least across a complete chromosome) or in discreet small coding chunks, regardless of where they occur in the genome?

    Does the comparison take into account the actual nucleotide sequence differences or does it, for example, treat “homologous” sequences as equivalent, thereby counting that section as completely similar?

    Does the comparison take into account methyl tags, histone tags, and other tags, or is it strictly a bottom-level, nucleotide-based comparison?

  116. 116
    Dionisio says:

    #95-98,105 follow up

    FYI: interesting lncRNA-related papers referenced in posts @1639-1649 within this link:

    http://www.uncommondescent.com.....ent-609847

    The more discoveries result from ongoing research, the more interesting the big picture turns.

    So much interesting research going on, one feels like a child in a toys store. 🙂

    Definitely exciting times to watch scientific research.

    BTW, I still don’t quite get this CD vs. UD debate.
    It seems a little confusing to me. Perhaps the terminology is a little vague? Dunno. Will have to set aside some spare time to learn more about it. Meanwhile, biological oscillators, feedback and feed forward loops in regulatory networks and stuff like that seem more interesting topics to study.

    PS. Strongly recommend watching the video lectures on systems biology by MIT (Boston) professor Jeff Gore and Weizmann Institute (Rehovot) professor Uri Alon. Don’t miss it!

  117. 117
    ThickPython says:

    @Bornagain77, #113:

    I respond in kind and will ignore your pointless “troll tripe” as well

    Well that’s not exactly surprising. As soon as you’re challenged, you run away.

    @HeKS, #114:

    Yes, it is the entire genome, “junk” included.

    @Eric Anderson, #115:

    I attempted to replicate the methodology that Jeff Tomkins used as closely as possible, so no, it’s not a linear comparison. Basically I took small sequences and BLASTed them against the corresponding chromosome to find the best hit.

    Yes, it takes into account both differences in individual nucleotides as well as indels. It’s a relatively conservative calculation method.

    No it doesn’t take into account any epigenetic tags – it is purely a nucleotide by nucleotide comparison.

  118. 118
    ThickPython says:

    Click here:

    https://www.dropbox.com/sh/dm2lgg0l93sjayv/AAATnWSJdER53EYEYZvcgiwma?dl=0

    … to see my paper as it was submitted to AiG in September 2014. Tomkins paper in October 2015 was in response to my paper.

  119. 119
    Querius says:

    Well that’s not exactly surprising. As soon as you’re challenged, you run away.

    Just as you and Professor Swamidass have ignored my challenge in #69.

    Science is supposed to be about observation, and you should be able to easily demonstrate the presumed efficacy of the evolutionary mechanism. Show us how cilia, flagella, legs, or whatever evolve in rapidly reproducing population of bacteria accelerated by ionizing radiation. You can set the radiation level equivalent to an equal number of human generations exposed to current levels of background radiation.

    Then, when you have the results, you can prove your point and win any number of awards, grants, and chairs!

    -Q

  120. 120
    Andre says:

    Mung

    Common descent as part a guided process? I buy that. Common descent Darwinian style? Don’t buy it. But you know that already ?

  121. 121
    Eric Anderson says:

    ThickPython @117/118:

    Awesome! Thanks for sharing the details and the materials.

  122. 122
    ThickPython says:

    @Querius, #119:

    Just as you and Professor Swamidass have ignored my challenge in #69.

    OH THAT CHALLENGE! I remember now – the one that wasn’t directed at me in the first place, the one that wasn’t in response to any claim that I had made, the one that required me to set up a laboratory at my own expense, and the one that required me to run an experiment that would clearly exceed the mutational load of any organism. Yes. I am ignoring that challenge.

    If you want to address anything I have claimed, then I’ll be happy to engage.

  123. 123
    gilthill says:

    @Gupio, #1

    You said “The simple observation of the frequency of synonymous mutations in different species is the strongest argument for common descent that we can imagine. I can’t really think of any possible alternative explanation for that simple and universal fact”.

    I don’t understand your point. Can you explain a little bit more how the frequency of synonymous mutations in different species indicates CD?

  124. 124
    Dionisio says:

    gilthill @123

    Please, you may want to review the spelling of the author of the first post in this thread.

    Thank you.

  125. 125
    bornagain77 says:

    Python, you accuse me of ‘running away’ when it was you yourself that ‘ran away’ from my ‘Gish gallop’. i.e. Hypocrisy thy name is Python!

    For instance, you ‘ran away’ from this at 24,,,

    ,,, Darwinists, simply have no solid scientific evidence whatsoever that it is possible to transform one kind of creature into another kind of creature simply by mutations to DNA alone. In other words, they have made an enormous, and completely erroneous, assumption that DNA sequences tell us something vitally important for the hypothesis of common ancestry when the fact of the matter is that DNA sequences tell us next to nothing about how it is even remotely possible to change one kind of creature into another kind of creature.
    http://www.uncommondescent.com.....ent-609483

    You want to make these grand claims about sequence comparisons in regards to common ancestry yet you have not even demonstrated your mechanism, i.e. random mutations to DNA, is even feasible as a mechanism. And indeed, as was pointed out in my ‘Gish gallop’, your preferred mechanism is grossly inadequate for the claims you are placing on it.

    You method of science reminds me of the alchemy of yesteryear.

    Darwinists haven’t even changed one type of bacteria into another type of bacteria by mutating DNA, (or by mutating anything else in the cell for that matter), much less have Darwinists changed one kind of creature of billions of trillions of protein molecules into another kind of creature of billions of trillions of protein molecules. You guys are putting the metaphysical cart way before the empirical horse

    Scant search for the Maker
    Excerpt: But where is the experimental evidence? None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of 20 to 30 minutes, and populations achieved after 18 hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another, in spite of the fact that populations have been exposed to potent chemical and physical mutagens and that, uniquely, bacteria possess extrachromosomal, transmissible plasmids. Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic to eukaryotic cells, let alone throughout the whole array of higher multicellular organisms.
    – Alan H. Linton – emeritus professor of bacteriology, University of Bristol.
    http://www.timeshighereducatio.....ode=159282

    Since Darwinists can’t demonstrate that it is even remotely feasible to change one creature into another creature by mutating DNA then that pretty much renders null and void yours, and Dawkins, entire ‘selfish gene’ scenario does it not?

    And I am far from the only one to find gross inadequacies in Dawkins’ entire self gene scenario. (references upon request)

    And seeing such a stark empirical poverty on your part for your primary claim, then why should I, or anyone else, take your claim seriously when your primary claim that it is possible to change one creature into another creature by randomly mutating DNA is empirically bankrupt? Can you at least even be honest with that simple fact?

    Despite all your bluff and bluster, and despite however badly you want atheistic materialism to be true, as far as the science itself is concerned, you don’t have a leg to stand on.

  126. 126
    mw says:

    Hi gpuccio, #1:

    ————————–
    “The simple observation of the frequency of synonymous mutations in different species is the strongest argument for common descent that we can imagine. I can’t really think of any possible alternative explanation for that simple and universal fact.”
    —————————

    Synonymous mutations, https://en.wikipedia.org/wiki/Synonymous_substitution

    Well, mutate a single possum cell from a non-possum cell, and previously, mutate dirt into a non possum by the ‘uncertainty’ of Darwinian processes?

    Where have we seen such strong arguments and certainty before; Darwin said:

    “It is incredible that all these facts should speak falsely. He who is not content to look, like a savage, at the phenomena of nature as disconnected, cannot any longer believe that man is the work of a separate act of creation.” (The Decent of Man, p. 386).

    Moses must have looked like, or as a savage? People must look like a savage when seeing documented evidence for Mount Sinai and divine law; and then believing in miracles? As for Jesus, Creator Saviour, in Judaeo-Christian belief, in Darwin’s terminology, demonstrated a savage behaviour!

    There is connectivity. But first, disconnectivity from Darwinism must seriously be considered, or at least open up the weakness of that theory in education.

    There are always two main choices for certainty in the present human psyche. We make a choice when all is said and done on the matter of the true origin of an opossum; but also believed, documented in rock, through divine law.

  127. 127
    bornagain77 says:

    Python, and if and when you practice science properly by putting the empirical evidence first instead of putting your atheistic/naturalistic metaphysics first as you are currently doing, then you will find out many wonderful things revealed by the empirical evidence. Wonderful things that are completely missed by those who falsely insist that ‘methodological naturalism’ is supposedly the ‘be all/end all’ a priori metaphysical/philosophical presumption of all of science.

    Methodological naturalism, the axiom of Materialism as it is applied to modern science, i.e. only materialistic/naturalistic answers are ever allowed, is the primary method of science taught in American universities. Yet, Materialism/Naturalism is not itself a finding of modern science but is a merely a unproven philosophy that is a-priorily imposed onto science. A completely unproven philosophy which makes the dogmatic assertion that only blind material processes generated the universe and everything in it, including ourselves.
    Materialism is thus in direct opposition to Theism which holds that God purposely created this universe and everything in it, including holding that God created us in His image.
    This dogmatic imposition of the philosophy of materialism, i.e. methodological naturalism, onto modern science is especially interesting since materialism had little to nothing to with the founding of modern science, but instead modern science was born out of the medieval Christian cultures of Europe by men who were by and large devoutly Christian in their beliefs.
    Moreover science, or more particularly the scientific method, in reality, only cares to relentlessly pursue the truth and could care less if the answer turns out to be a materialistic one or not. Ironically, since truth itself is a transcendent entity which is not reducible to purely material/natural entity then Methodological Naturalism actually precludes ‘the truth’ from ever being reached by science!
    Imposing materialistic answers onto the scientific method beforehand, methodological naturalism, is especially problematic in these questions of origins, since we are indeed questioning the materialistic philosophy itself. i.e. We are asking the scientific method to answer this very specific question, “Did God create the universe and us or did blind material processes create the universe and us?” When we realize that this is the actual question we are seeking an answer to within the scientific method, then of course it is readily apparent we cannot impose strict materialistic answers onto the scientific method prior to investigation.
    When looking at the evidence from modern science in this light we find out many interesting things which scientists, who have been blinded by the philosophy of materialism, miss.
    This is because the materialistic and Theistic philosophy make, and have made, several natural contradictory predictions about what type of science evidence we will find.
    These contradictory predictions, and the evidence we have found by modern science, can be tested against one another to see if either materialism or Theism is true.

    Here are a few comparisons:

    Theism compared to Materialism/Naturalism – a comparative overview of the major predictions of each philosophy – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1139512636061668/?type=2&theater

    1. Naturalism/Materialism predicted space-time energy-matter always existed. Theism predicted space-time energy-matter were created. Big Bang cosmology now strongly indicates that time-space energy-matter had a sudden creation event approximately 14 billion years ago.

    2. Naturalism/Materialism predicted that the universe is a self sustaining system that is not dependent on anything else for its continued existence. Theism predicted that God upholds this universe in its continued existence. Breakthroughs in quantum mechanics reveal that this universe is dependent on a ‘non-local’, beyond space and time, cause for its continued existence.

    3. Naturalism/Materialism predicted that consciousness is an ‘emergent property’ of material reality and thus should have no particularly special position within material reality. Theism predicts consciousness precedes material reality and therefore, on that presupposition, consciousness should have a ‘special’ position within material reality. Quantum Mechanics reveals that consciousness has a special, even a central, position within material reality. –

    4. Naturalism/Materialism predicted the rate at which time passed was constant everywhere in the universe. Theism predicted God is eternal and is outside of time. – Special Relativity has shown that time, as we understand it, is relative and comes to a complete stop at the speed of light. (Psalm 90:4 – 2 Timothy 1:9) –

    5. Naturalism/Materialism predicted the universe did not have life in mind and that life was ultimately an accident of time and chance. Theism predicted this universe was purposely created by God with man in mind. Scientists find the universe is exquisitely fine-tuned for carbon-based life to exist in this universe. Moreover it is found, when scrutinizing the details of physics and chemistry, that not only is the universe fine-tuned for carbon based life, but is specifically fine-tuned for life like human life (R. Collins, M. Denton).-

    6. Naturalism/Materialism predicted complex life in this universe should be fairly common. Theism predicted the earth is extremely unique in this universe. Statistical analysis of the hundreds of required parameters which enable complex organic life to be possible on earth gives strong indication the earth is extremely unique in this universe (G. Gonzalez; Hugh Ross). –

    7. Naturalism/Materialism predicted it took a very long time for life to develop on earth. Theism predicted life to appear abruptly on earth after water appeared on earth (Genesis 1:10-11). Geochemical evidence from the oldest sedimentary rocks ever found on earth indicates that complex photosynthetic life has existed on earth as long as water has been on the face of earth. –

    8. Naturalism/Materialism predicted the first life to be relatively simple. Theism predicted that God is the source for all life on earth. The simplest life ever found on Earth is far more complex than any machine man has made through concerted effort. (Michael Denton PhD) –

    9. Naturalism/Materialism predicted the gradual unfolding of life would (someday) be self-evident in the fossil record. Theism predicted complex and diverse animal life to appear abruptly in the seas in God’s fifth day of creation. The Cambrian Explosion shows a sudden appearance of many different and completely unique fossils within a very short “geologic resolution time” in the Cambrian seas. –

    10. Naturalism/Materialism predicted there should be numerous transitional fossils found in the fossil record, Theism predicted sudden appearance and rapid diversity within different kinds found in the fossil record. Fossils are consistently characterized by sudden appearance of a group/kind in the fossil record(disparity), then rapid diversity within that group/kind, and then long term stability and even deterioration of variety within the overall group/kind, and within the specific species of the kind, over long periods of time. Of the few dozen or so fossils claimed as transitional, not one is uncontested as a true example of transition between major animal forms out of millions of collected fossils. –

    11. Naturalism/Materialism predicted animal speciation should happen on a somewhat constant basis on earth. Theism predicted man was the last species created on earth – Man (our genus ‘modern homo’ as distinct from the highly controversial ‘early homo’) is the last generally accepted major fossil form to have suddenly appeared in the fossil record. (Tattersall; Luskin)–

    12. Naturalism/Materialism predicted that the separation of human intelligence from animal intelligence ‘is one of degree and not of kind’(C. Darwin). Theism predicted that we are made in the ‘image of God’- Despite an ‘explosion of research’ in this area over the last four decades, human beings alone are found to ‘mentally dissect the world into a multitude of discrete symbols, and combine and recombine those symbols in their minds to produce hypotheses of alternative possibilities.’ (Tattersall; Schwartz). Moreover, both biological life and the universe itself are found to be ‘information theoretic’ in their foundational basis.

    13. Naturalism/Materialism predicted much of the DNA code was junk. Theism predicted we are fearfully and wonderfully made – ENCODE research into the DNA has revealed a “biological jungle deeper, denser, and more difficult to penetrate than anyone imagined.”. –

    14. Naturalism/Materialism predicted a extremely beneficial and flexible mutation rate for DNA which was ultimately responsible for all the diversity and complexity of life we see on earth. Theism predicted only God created life on earth – The mutation rate to DNA is overwhelmingly detrimental. Detrimental to such a point that it is seriously questioned whether there are any truly beneficial, information building, mutations whatsoever. (M. Behe; JC Sanford) –

    15. Naturalism/Materialism predicted morality is subjective and illusory. Theism predicted morality is objective and real. Morality is found to be deeply embedded in the genetic responses of humans. As well, morality is found to be deeply embedded in the structure of the universe. Embedded to the point of eliciting physiological responses in humans before humans become aware of the morally troubling situation and even prior to the event even happening.

    16. Naturalism/Materialism predicted that we are merely our material bodies with no transcendent component to our being, and that we die when our material bodies die. Theism predicted that we have minds/souls that are transcendent of our bodies that live past the death of our material bodies. Transcendent, and ‘conserved’, (cannot be created or destroyed), ‘non-local’, (beyond space-time matter-energy), quantum entanglement/information, which is not reducible to matter-energy space-time, is now found in our material bodies on a massive scale (in every DNA and protein molecule).

    As you can see when we remove the artificial imposition of the materialistic philosophy (methodological naturalism), from the scientific method, and look carefully at the predictions of both the materialistic philosophy and the Theistic philosophy, side by side, we find the scientific method is very good at pointing us in the direction of Theism as the true explanation. – In fact science is even very good at pointing us to Christianity as the solution to the much sought after ‘theory of everything’

    The Resurrection of Jesus Christ from Death as the “Theory of Everything” – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1143437869002478/?type=2&theater

    Verse and Music:

    1 Thessalonians 5:21
    but test everything; hold fast what is good.

    K-LOVE – For King & Country “The Proof Of Your Love” LIVE
    https://www.youtube.com/watch?v=pr9YVD05x8M

  128. 128
    Origenes says:

    Cornelius Hunter:
    “Chimp-Human Alternate Splicing Differences

    … When a gene is transcribed, the transcript contains both the exons and introns. It is then spliced by a complicated spliceosome machine that removes the introns from the gene copy and glues the exons together.

    One of the features of the exon/intron genetic architecture is that it allows for alternative splicing schemes. In fact, incredibly, a given gene can have thousands of different forms depending on how the spliceosome machine edits the gene.

    … We have an enormous alternative splicing program in our cells, far more than chimps have. And this is another inconsistency with evolutionary theory.

    … there are many thousands of these gene-splicing changes that would have to evolve. And unlike bacteria whose populations are large and generation times are short, our gene splicing changes would have to evolve in smaller populations with longer generation times.
    It is difficult to see how evolution would have the resources to make this happen. The problem quickly becomes astronomically improbable if groups of genes would need to implement their new splicing logic together. And how could that not be the case?

    In fact, even if only the order of implementing splicing for a small number of genes is important, the problem quickly becomes astronomically improbable. And again, how could that not be the case?

    But this is only the beginning. In addition to the fact that the evolution of our enormous gene splicing changes is unlikely, it also represents an enormous serendipity problem. We would have to say that random mutations constructed complicated genes, with exons and introns and splicing codes, and the incredible splicing machinery, which, it would just so happen, would luckily be just what was needed to evolve humans.

    It is even worse than this when one considers the exons themselves. Those random mutations would have divided the genetic instructions into so many exons, and it just so happened that they would be the right building blocks that, when rearranged, would lead to humans. The serendipity is astronomical here.

    Imagine if you were building a tricycle and your friend modified each part you had crafted (not adding anything), and now the parts fit together to construct the space shuttle rocket motor.

    //
    For me, the bolded paragraph offers a valuable and comprehensive way to look at the DNA similarities between chimps and humans.

  129. 129
    bornagain77 says:

    Origenes, as to Hunter’s comment here:

    “The problem quickly becomes astronomically improbable if groups of genes would need to implement their new (alternative) splicing logic together. And how could that not be the case?”

    And indeed, that is exactly the case that is found:

    ,,,Alternative splicing,,, may contribute to species differences – December 21, 2012
    Excerpt: After analyzing vast amounts of genetic data, the researchers found that the same genes are expressed in the same tissue types, such as liver or heart, across mammalian species. However, alternative splicing patterns—which determine the segments of those genes included or excluded—vary from species to species.,,,
    The results from the alternative splicing pattern comparison were very different. Instead of clustering by tissue, the patterns clustered mostly by species. “Different tissues from the cow look more like the other cow tissues, in terms of splicing, than they do like the corresponding tissue in mouse or rat or rhesus,” Burge says. Because splicing patterns are more specific to each species, it appears that splicing may contribute preferentially to differences between those species, Burge says,,,
    Excerpt of Abstract: To assess tissue-specific transcriptome variation across mammals, we sequenced complementary DNA from nine tissues from four mammals and one bird in biological triplicate, at unprecedented depth. We find that while tissue-specific gene expression programs are largely conserved, alternative splicing is well conserved in only a subset of tissues and is frequently lineage-specific. Thousands of previously unknown, lineage-specific, and conserved alternative exons were identified;
    http://phys.org/news/2012-12-e.....wires.html

    Alternative Splicing Codes are Species Specific
    https://docs.google.com/document/d/1UMbNM8V2b7mRzPJt05mlev3UO4SG1bMTV5wkNunezjY/edit

  130. 130
    gpuccio says:

    mw at #126:

    I am not sure that I understand the sense of your intervention, especially as addressed to me.

    Why do you link Wikipedia about synonymous mutations? I know what they are, otherwise I would not have based my argument for descent on them.

    Then you say:

    “Well, mutate a single possum cell from a non-possum cell, and previously, mutate dirt into a non possum by the ‘uncertainty’ of Darwinian processes?”

    But, have you really read my post #1? In no way I rely on “darwinian processes” for anything.

    I quote myself:

    “To be clear, and to avoid the usual misunderstandings, what I am discussing here is descent with designed modifications, and nothing else. We all agree that all the new complex information which arises in all species is designed, and cannot be explained by any neo-darwinian theory, or more generally by any non design theory which does not imply the explicit intervention, in time and space, of some conscious, intelligent and purposeful being as a designer. Not even a single new complex protein can be explained without a designer.

    That has nothing to do with descent. Descent just means that we can safely infer that the proteins which are conserved in distant species, and retain similar function, show differences (especially synonymous mutations) which:

    a) do not change their function

    b) are grossly proportional to the chronological distance between the species.

    IOWs, if we accept descent for the information which is maintained in different species, then the pattern of non functional differences (such as synonymous mutations) can be explained by physical descent and neutral variation.

    I am not aware of any other reasonable explanation. Why should the synonymous mutations rate be grossly proportional to chronological distance? If you have different explanations, please provide them.

    As the pattern of synonymous mutations rate is rather regular, and extremely widespread, I really believe that we need a scientific explanation for it.

    Of course, all new information in species is designed, and therefore has nothing to do with descent or “darwinian mechanisms”. Nothing at all.

    That is what I have stated from the beginning, “to be clear, and to avoid the usual misunderstandings”.

    But perhaps that is really an impossible task.

  131. 131
    gpuccio says:

    gilthill:

    “I don’t understand your point. Can you explain a little bit more how the frequency of synonymous mutations in different species indicates CD?”

    Yes, I can, but I need a little bit of free time! 🙂

    The general idea you can find in my post #130. But I want to give you real examples.

    Let’s say that the synonymous mutations rate, which can be easily and objectively computed when we compare two similar proteins from different species, is lower if we compare, say, lose and human, and higher if we compare, say, a bony fish and humans. That is the simple basic idea. But I will give you real examples, as soon as possible.

  132. 132
    bornagain77 says:

    gp as to:

    “To be clear, and to avoid the usual misunderstandings, what I am discussing here is descent with designed modifications, and nothing else.”

    And as with the ‘and then a miracle happens’ cartoon would you, or Torley, care to be a little more specific? Leaving out how much ‘design modification’ is implemented exactly when by God, as you and Torley both have done in your explanation, is a fairly serious chasm in your explanation don’t you agree?

  133. 133
    mw says:

    Thank you gpuccio, #131, for a scholarly reply.

    I appreciate your valuable time and efforts in the matter.

    Still, by whatever means, construct an opossum from zero.

    Even by placing divine intelligence in the mix does not prove a higher intelligence constructed an opossum, because we are surely venturing in the realms of theology, and as some would say; “the Queen of science.”

    Still, I see little wrong, in my opinion, in trying to explore such consequences.

  134. 134
    gilthill says:

    Gpuccio #126
    Thanks you very muche for your answer.
    I myself need somme more free time to think about this issue.I will be happy to reads your real exemples.

  135. 135
    bornagain77 says:

    To highlight the unfalsifiable nature of the hypothesis Common ancestry once again.

    Darwinists and Theistic Evolutionists both hold to the belief that sequence, and morphological, similarity between supposedly closely related species as undeniable evidence for common ancestry. Yet by the same reasoning, sequence, and morphological, similarity of supposedly widely divergent species should falsify that particular hypothesis of theirs. Yet the hypothesis of common ancestry is protected from falsification by the invocation of what is called ‘convergent evolution’.

    Thus, similar sequences in either supposedly closely related species or distantly related species both end up confirming evolution. What should be needless to say, this practice of both confirming and dis-confirming evidence supporting a theory is not science but is the sure mark that we are dealing with a unfalsifiable pseudo-science.

    Notes:

    Karl Popper’s Falsification – video
    https://www.youtube.com/watch?v=wf-sGqBsWv4

    “In so far as a scientific statement speaks about reality, it must be falsifiable; and in so far as it is not falsifiable, it does not speak about reality.”
    Karl Popper – The Two Fundamental Problems of the Theory of Knowledge (2014 edition), Routledge

    Darwinism Versus the Octopus: An Evolutionary Dilemma – Eric Metaxas – September 08, 2015
    Excerpt: What’s the difference between evolutionary theory and an octopus? Well, one is a slippery, color-changing escape artist that can get out of any tough situation and the other is an aquatic invertebrate.,,,
    The key to this uncanny intelligence is the octopus’ so-called “alien” nervous system, brain, and eyes. But these features are not alien to the animal kingdom at all. In fact, they’re quite common in higher vertebrates. The octopus genome shares key similarities with ours, including the development of high-powered brains and “camera eyes” with a cornea, lens, and retina.
    Now here’s the problem for evolution: according to Neo-Darwinists, we’re not related to octopi—at least not within the last several hundred million years. That means all of these genes, complex structures, and incredible capabilities came about twice.
    The researchers who sequenced the octopus genome call this “a striking example of convergent evolution,” or the supposed tendency of unrelated creatures to develop the same traits in response to environmental pressures. Isn’t that just a fancy way of saying a miracle happened twice?
    But the octopus isn’t the only such miracle. “Convergent evolution” is all over nature, from powered flight evolving three times to each continent having its own version of the anteater. Think about that. As one delightfully un-self-conscious “Science Today” cover put it, convergent evolution is “nature discover[ing] the same design over and over.” Well, good for nature!
    But as Luskin argues, there’s a better explanation for a tentacled mollusk having a mammal’s brain and human eyes. And that explanation is common design by an intelligent Engineer. And like all good engineers, this this one reused some of His best designs.
    Now that explanation isn’t going to satisfy Darwinian naturalists. And they’ll probably keep on invoking “convergent evolution” when faced with impossible coincidences in nature.
    But hopefully knowing a more straightforward explanation leaves you forearmed—or should I said “eight-armed”?
    http://www.christianheadlines......lemma.html

    Newly Discovered Convergent Genetic Evolution Between Bird and Human Vocalization Poses a Severe Challenge to Common Ancestry – Casey Luskin – December 15, 2014
    Excerpt: “We’ve known for many years that the singing behavior of birds is similar to speech in humans — not identical, but similar -,,, “But we didn’t know whether or not those features were the same because the genes were also the same.”
    “Now scientists do know, and the answer is yes — birds and humans use essentially the same genes to speak.”,,,
    “there is a consistent set of just over 50 genes,,,”
    “These changes were not found in the brains of birds that do not have vocal learning and of non-human primates that do not speak,”
    So certain birds and humans use the same genes for vocalization — but those genetic abilities are absent in non-human primates and birds without vocal learning? If not derived from a common ancestor, as they clearly were not, how did the genes get there? This kind of extreme convergent genetic evolution points strongly to intelligent design.
    http://www.evolutionnews.org/2.....92041.html

    Convergent sequence evolution between echolocating bats and dolphins – Liu et al (2010)
    Excerpt: We previously reported that the Prestin gene has undergone sequence convergence among unrelated lineages of echolocating bat [3]. Here we report that this gene has also undergone convergent amino acid substitutions in echolocating dolphins,
    http://www.cell.com/current-bi.....%2902073-9

    The echolocation abilities of bats and whales, though different in their details, rely on the same changes to the same gene – Prestin. These changes have produced such similar proteins that if you drew a family tree based on their amino acid sequences, bats and toothed whales would end up in the same tight-knit group, to the exclusion of other bats and whales that don’t use sonar.
    http://blogs.discovermagazine......XXadkbcBCA

    Bothersome Bats and Other Pests Disturb the “Tree of Life” – Casey Luskin – December 5, 2012
    Excerpt: But this is hardly the only known example of molecular convergent evolution. In his book The Cell’s Design, chemist and Darwin-skeptic Fazale Rana reviewed the technical literature and documented over 100 reported cases of convergent genetic evolution. Each case shows an example where biological similarity — even at the genetic level — is not the result of inheritance from a common ancestor.
    http://www.evolutionnews.org/2.....67121.html

    Convergent evolution seen in hundreds of genes – Erika Check Hayden – 04 September 2013
    Excerpt: “These results imply that convergent molecular evolution is much more widespread than previously recognized,” says molecular phylogeneticist Frédéric Delsuc at the The National Center for Scientific Research (CNRS) at the University of Montpellier in France, who was not involved in the study. What is more, he adds, the genes involved are not just the few, obvious ones known to be directly involved in a trait but a broader array of genes that are involved in the same regulatory networks.
    http://www.nature.com/news/con.....es-1.13679

  136. 136
    bornagain77 says:

    Convergent evolution’ (homology in unexpected places) is found to be much more widespread than originally thought. Far more often than would be expected under the neo-Darwinian framework.

    “Despite its complexity, C4 photosynthesis is one of the best examples of ‘convergent evolution’, having evolved more than 50 times in at least 18 plant families (Sage 2004; Conway Morris 2006).”
    http://mbe.oxfordjournals.org/.....9.full.pdf

    “The reason evolutionary biologists believe in “40 known independent eye evolutions” isn’t because they’ve reconstructed those evolutionary pathways, but because eyes don’t assume a treelike pattern on the famous Darwinian “tree of life.” Darwinists are accordingly forced, again and again, to invoke convergent “independent” evolution of eyes to explain why eyes are distributed in such a non-tree-like fashion.
    This is hardly evidence against ID. In fact the appearance of eyes within widely disparate groups speaks eloquently of common design. Eyes are a problem, all right — for Darwinism.”
    http://www.evolutionnews.org/2.....83441.html

    Simon Conway Morris has a website documenting hundreds, if not thousands, of examples of ‘convergence’:

    Map Of Life – Simon Conway Morris
    http://www.mapoflife.org/browse/

    Simon Conway Morris: “Fossil evidence demands a radical rewriting of evolution.” – March 2012
    Excerpt: “The idea is this: that convergence – the tendency of very different organisms to evolve similar solutions to biological problems – is not just part of evolution, but a driving force. To say this is an unconventional view would be something of an understatement.
    http://www.uncommondescent.com.....evolution/

  137. 137
    bill cole says:

    Gpuccio

    “To be clear, and to avoid the usual misunderstandings, what I am discussing here is descent with designed modifications, and nothing else. We all agree that all the new complex information which arises in all species is designed, and cannot be explained by any neo-darwinian theory, or more generally by any non design theory which does not imply the explicit intervention, in time and space, of some conscious, intelligent and purposeful being as a designer. Not even a single new complex protein can be explained without a designer.”

    I certainly agree with your point here. My only real problem with common decent is that it is misleading the public because when used by evolutionary biologists it implies that no design or other unknown mechanism was needed. It infers that a new specie can arise simply from random generational change in isolating populations. As you said this will not even evolve one complex protein due to the massive sequential space in DNA and Proteins.

  138. 138
    Eric Anderson says:

    Origenes @128 (Hunter actually):

    This is an excellent point that is so often missed in the comparative DNA studies. And the disconnect flows in large measure from the blatantly-wrong-but-still-often-propagandized Central Dogma that views DNA as prosecutor, judge, and jury — with all biological power and influence flowing just from the sequencing of the nucleotides itself.

    A much better way to think of DNA is as a database. Or if we want to talk about mechanical/chemical machines, as a parts warehouse. Two contractors can walk into Home Depot, having the exact 100% identical access to tools and parts, and end up building wildly different houses with remarkably different features.

    One of the very ironic things about claims of human-chimp DNA similarity is that the claims inadvertently underscore the fact that the differences between the organisms are not just in the DNA. Even if humans and chimps had 100% similar DNA, down to the very last nucleotide, it would not teach us anything particularly concrete about organismal similarity, or descent, or evolutionary relationships.

    What evolution must explain fundamentally, what is purports to be able to explain, is the differences between organisms — how new structures and capabilities and traits arise. That is what Darwin was hoping to explain. Showing that B descended from A and didn’t change much in the process is not an impressive or even a particularly relevant observation for demonstrating the power of the evolutionary mechanism.

  139. 139
    bornagain77 says:

    Not to stir up a hornets nest, but,,,

    Vincent Torley Thinks I Have Egg on My Face
    Ann Gauger June 10, 2016
    http://www.evolutionnews.org/2.....02913.html

  140. 140
    wd400 says:

    And the disconnect flows in large measure from the blatantly-wrong-but-still-often-propagandized Central Dogma that views DNA as prosecutor, judge, and jury — with all biological power and influence flowing just from the sequencing of the nucleotides itself.

    That’s not the central dogma of molecular biology (which only states that sequence information flows from DNA to protein and not backwards).

    Buy what, if not DNA sequence, controls biological function? I guess you are going to say methylation, transcription factors functional RNA etc, but all of those are encoded by DNA.

  141. 141
    bornagain77 says:

    “Buy what, if not DNA sequence, controls biological function?”

    spoken like a true Darwinian dogmatist. Never mind that DNA is found not to be ‘selfish’, It is simply unthinkable for him to even consider looking elsewhere for ‘functional control’ of biology. Such as say looking to the organism as a whole that the trillions upon trillions of DNA and protein molecules are dedicated to keeping alive for precisely a life time and not a moment longer.(Talbott) No looking to the organism as a whole would be too obvious!

    Notes:

    Ask an Embryologist: Genomic Mosaicism – Jonathan Wells – February 23, 2015
    Excerpt: humans have a “few thousand” different cell types. Here is my simple question: Does the DNA sequence in one cell type differ from the sequence in another cell type in the same person?,,,
    The simple answer is: We now know that there is considerable variation in DNA sequences among tissues, and even among cells in the same tissue. It’s called genomic mosaicism.
    In the early days of developmental genetics, some people thought that parts of the embryo became different from each other because they acquired different pieces of the DNA from the fertilized egg. That theory was abandoned,,,
    ,,,(then) “genomic equivalence” — the idea that all the cells of an organism (with a few exceptions, such as cells of the immune system) contain the same DNA — became the accepted view.
    I taught genomic equivalence for many years. A few years ago, however, everything changed. With the development of more sophisticated techniques and the sampling of more tissues and cells, it became clear that genetic mosaicism is common.
    I now know as an embryologist,,,Tissues and cells, as they differentiate, modify their DNA to suit their needs. It’s the organism controlling the DNA, not the DNA controlling the organism.
    http://www.evolutionnews.org/2.....93851.html

    Marching to our own sequence: Study finds DNA replication timing varies among people – Nov 13, 2014
    Excerpt: A new study from geneticists at Harvard Medical School and the Broad Institute of Harvard and MIT has found that this replication plan—including where the origin points are and in what order DNA segments get copied—varies from person to person.
    The study also identifies the first genetic variants that orchestrate replication timing.
    “Everyone’s cells have a plan for copying the genome. The idea that we don’t all have the same plan is surprising and interesting,” said Steven McCarroll, assistant professor of genetics at HMS, director of genetics for the Stanley Center for Psychiatric Research at the Broad and senior author of the paper.
    “It’s a new form of variation in people no one had expected,” said first author Amnon Koren, postdoctoral fellow at HMS and the Broad. “That’s very exciting.”
    http://phys.org/news/2014-11-s.....eople.html

    “Physiology Is Rocking the Foundations of Evolutionary Biology”: Another Peer-Reviewed Paper Takes Aim at Neo-Darwinism – Casey Luskin March 31, 2015
    Excerpt: Noble doesn’t mince words:
    “It is not only the standard 20th century views of molecular genetics that are in question. Evolutionary theory itself is already in a state of flux (Jablonka & Lamb, 2005; Noble, 2006, 2011; Beurton et al. 2008; Pigliucci & Muller, 2010; Gissis & Jablonka, 2011; Shapiro, 2011). In this article, I will show that all the central assumptions of the Modern Synthesis (often also called Neo-Darwinism) have been disproved.”
    Noble then recounts those assumptions: (1) that “genetic change is random,” (2) that “genetic change is gradual,” (3) that “following genetic change, natural selection leads to particular gene variants (alleles) increasing in frequency within the population,” and (4) that “inheritance of acquired characteristics is impossible.” He then cites examples that refute each of those assumptions,,,
    He then proposes a new and radical model of biology called the “Integrative Synthesis,” where genes don’t run the show and all parts of an organism — the genome, the cell, the body plan, everything — is integrated.
    http://www.evolutionnews.org/2.....94821.html

    Bonus note:

    Genes and Organisms: Improvising the Dance of Life – Stephen L. Talbott – Nov. 10, 2015
    Excerpt: The performances of countless cells in your body are redirected and coordinated as part of a global narrative for which no localized controller exists. This redirection and coordination includes a unique choreography of gene expression in each individual cell. Hundreds or thousands of DNA sequences move (or are moved) within vast numbers of cell nuclei, and are subjected to extraordinarily nuanced, locally modulated chemical activity so as to contribute appropriately to bodily requirements that are nowhere codified — least of all in those DNA sequences.,,,
    DNA in its larger matrix
    You may recall from my earlier article, “Getting Over the Code Delusion” (Talbott 2010), that packing DNA into a typical cell nucleus is like packing about 24 miles of very thin, double-stranded string into a tennis ball, with the string cut up (in the normal human case) into 46 pieces, corresponding to our 46 chromosomes.
    To locate a protein-coding gene of typical size within all that DNA is like homing in on a one-half-inch stretch within those 24 miles. Or, rather, two relevant half-inch stretches located on different pieces of string, since we typically have two copies of any given gene. Except that sometimes one copy differs from the other and one version is not supposed to be expressed, or one version needs to be expressed more than the other, or the product of one needs to be modified relative to the other. So part of the job may be to distinguish one of those half-inch stretches from the other. “Decisions” everywhere, it seems.
    But no such decisions are made in a vacuum. As it happens, the chromosome does not consist of a naked DNA double helix. Our DNA, rather, is bound up with a massive, intricate, and dynamic protein-RNA-small molecule complex (called chromatin) that is as fully “informative” for the cell as the DNA sequence itself — and, you might say, much more active and directive.,,,
    the cell, by managing the shifting patterns of the chromatin infrastructure within which DNA is embedded, brings our chromosomes into movement on widely varying scales. These include large looping movements that put particular genes into connection with essential regulatory sequences and with other, related genes (that is, with other one-half inch stretches of our “24 miles of string in a tennis ball”).,,,
    A gene is not in any case the kind of rigidly defined entity one might hope to calculate with. As a functional unit appropriate to current circumstances, it must be cobbled together by the cell according to the needs of the moment. There is no neatly predefined path to follow once the cell has located the “right” half inch or so of string, or once it has done whatever is necessary to bring that locus into proper relation with other chromosomal loci participating in the same “dance”.
    One issue has to do with the fact that there are two strands in the DNA double helix and, starting from any particular point, it is possible to transcibe either of two DNA sequences in either of two directions: “forward” along one strand, or “backward” along the other. This yields two completely different products. One of them is very likely not even a protein-coding RNA, and yet it may still play a vital role in gene expression and in cellular processes more generally.
    And even when the cell would proceed in one particular direction, it must “choose” the exact point in the genetic sequence at which to begin. Different starting points can yield functionally distinct results. “Many studies focusing on single genes have shown that the choice of a specific transcription start site has critical roles during development and cell differentiation, and aberrations in . . . transcription start site use lead to various diseases including cancer, neuropsychiatric disorders, and developmental disorders”.8,,,
    The (protein) enzyme that transcribes DNA into RNA is RNA polymerase12. The enzyme certainly does not work alone, however, and its task is by no means cut-and-dried. To begin with, its critical interactions with various elements of the pre-initiation complex help determine whether and exactly where transcription will begin, if it is to begin at all. Then, after those “decisions” have been made, RNA polymerase moves along the double helix transcribing the sequence of genetic “letters” into the complementary sequence of an RNA.
    Throughout this productive journey, which is called elongation, the RNA polymerase still keeps good and necessary company. Certain co-activators modify it during its transit of a genetic locus, and these modifications not only enable transcription elongation to begin, but also provide binding sites for yet other proteins that will cooperate throughout the transcription journey.,,,
    Finally — and mirroring all the possibilities surrounding initiation of gene transcription — there are the issues relating to its termination. Again, they are far too many to mention here. Transcription may conclude at a more or less canonical terminus, or at an alternative terminus, or it may proceed altogether past the gene locus, even to the point of overlapping what, by usual definitions, would be regarded as a separate gene farther “downstream”. The cell has great flexibility in determining what, on any given occasion, counts as a gene, or transcriptional unit.
    The last part of the transcribed gene is generally non-protein-coding, but nevertheless contains great significance. Examining this region in a single gene, a research team recently identified “at least 35 distinct regulatory elements” to which other molecules can bind.13 Further regulatory potentials arise from yet more binding sites on the customized “tail” that the cell adds to the RNA immediately upon conclusion of its transcription.
    Proteins and other molecules that bind to the various regulatory elements of the non-protein-coding portion of the transcript do so in a context-sensitive manner, where cell and tissue type, phase of the cell cycle, developmental stage, location of the RNA within the cell, and environmental factors, both intra- and extra-cellular, may all play a role. These converging influences can change the stability of the RNA, change its localization within the cell, and change the efficiency of its translation into protein, among other possibilities.,,,
    What is generally considered the post-transcriptional modulation of gene expression actually begins during transcription proper. A prime example has to do with what happens partly as a result of the pauses during elongation.
    Cells don’t just passively accept the RNAs that emerge from the transcription process, but rather “snip and stitch” them via an elaborate procedure known as RNA splicing. It happens that the cutting out and knitting together of selected pieces typically begins before the RNA is fully transcribed, and the rhythm of pauses during elongation has an important influence upon which pieces form the mature transcript.
    This splicing operation, which is applied to nearly all human RNAs, is performed by the spliceosome, consisting of a few non-protein-coding RNAs and over 300 cooperating proteins, and is hardly less exacting in its requirements than, say, brain surgery.
    For the vast majority of human genes the operation can be performed in different ways, yielding distinct proteins (called isoforms) from a single RNA derived from a single DNA sequence. This is called alternative splicing, and it would be hard to find anything in human development, disease etiology, or normal functioning that is not dependent in one way or another on the effectiveness of this liberty the cell takes with its gene products.
    But RNA splicing is hardly the end of it. Through RNA editing the cell can add, delete, or substitute individual “letters” of the RNA sequence.15 Or, leaving the letters in place, the cell can chemically modify them in any of over one hundred different ways.16 ,,,
    Eventually, a protein-coding RNA needs to be translated into protein. This happens by means of large molecular complexes called “ribosomes”. Just as with gene transcription, there are many associated factors that must work together to bring about the initiation of translation, many that cooperate with the ribosome during translation, and yet others that play a role in modifying, localizing, or otherwise regulating the newly produced protein.
    The overall picture of gene expression is one of unsurveyable complexity in the service of remarkably effective living processes.,,,
    A decisive problem for the classical view of DNA is that “as cells differentiate and respond to stimuli in the human body, over one million different proteins are likely to be produced from less than 25,000 genes”.30 Functionally, in other words, you might say that we have over a million genes.,,,
    http://www.natureinstitute.org.....nes_29.htm

  142. 142
    Origenes says:

    WD400: But what, if not DNA sequence, controls biological function? I guess you are going to say methylation, transcription factors functional RNA etc, but all of those are encoded by DNA.

    WD400, I would rather say that some things cannot be explained bottom-up.

    For instance, given that blind particles don’t think, how can they be in control of thought?
    Put another way:
    if blind particles are in control of thought, how can rationality exist?
    If blind particles control our behavior, how can freedom, responsibility and rationality exist?
    If blind particles constitute consciousness, how can consciousness be anything other than an illusion?
    If consciousness, rationality, freedom and responsibility are non-existent, how can science exist?

  143. 143
    bill cole says:

    WD40

    Buy what, if not DNA sequence, controls biological function? I guess you are going to say methylation, transcription factors functional RNA etc, but all of those are encoded by DNA.

    An exception I am aware of is vitamin d3 which is a mission critical transcription activating molecule. It is first synthesized in the skin by uv light interacting with cholesterol. It moves to the liver where an OH is added and then moves to the kidney were another OH is added. The final steroid is called calcitriol which goes inside our cells and works to down regulate the cell cycle. If your blood vitamin d levels are low your are susceptible to many diseases including cancer.

  144. 144
    gpuccio says:

    gilthill and others:

    As promised, here are real examples. I will keep it as simple as possible.

    Some definitions:

    ka: the rate of nonsynonymous substitutions between two or more similar sequences in different species.

    ks: the rate of synonymous substitutions between two or more similar sequences in different species.

    ka/ks: the ratio between the two.

    The general concept:

    ka is very different from protein to protein: the more the protein is functionally constrained, the lower the ka, even between very distant species. IOWs, non synonymous substitutions are often functionally deleterious and therefore are eliminated by negative, purifying selection.

    ks is similar and relatively constant between definite species, and grossly proportional to the chronological distance between the two species. IOWs, ks measures neutral variation, which happens at rather constant rates, and therefore is proportional to time.

    ka/ks: as a consequence, the lower the ratio, the higher the functional constraint, and therefore the sequence conservation. The more the value is lower than 1, the higher the functional conservation.

    Let’s go to some numbers:

    Two proteins:

    a) p53, a very important transcription factor

    b) myoglobin

    Three species:

    1) humans, which we will use as constant comparison

    2) one mammmal, the mouse

    3) one lizard, jekko japonicus

    Here are the values:

    Human vs mouse p53:

    ka = 0.1499108

    ks = 0.5899543

    ka/ks = 0.254105784

    Human vs jekko japonicus p53:

    ka = 0.4617699

    ks = 2.0269440

    ka/ks = 0.227815815

    And now, myoglobin:

    Human vs mouse myoglobin:

    ka = 0.09214577

    ks = 0,6423085

    ka/ks = 0,1434603

    Human vs jekko japonicus myoglobin:

    ka = 0,18517071

    ks = 1.4909851

    ka/ks = 0.124193535

    Simple comments:

    1) Myoglobin is slightly more conserved than p53 (lower ka/ks)

    2) Ks is very similar for the two proteins in mouse (0.5899543 vs 0,6423085) and is very similar in jekko for the two proteins (2.0269440 vs 1.4909851), but it is definitely higher in the human-jekko comparison vs the human- mouse comparison (3,44 times higher for p53, 2,32 times higher for myoglobin).
    That means that, even with our small sample of two proteins, ks is about 3 times higher between humans and lizards, than it is between humans and rodents.

    Now, how do you explain that? And believe me, the results would be confirmed by further comparisons.

    Now, the human lineage is thought to have split from rodents about 80 million years ago.

    On the contrary, the split between human lineage and lizards should be about 300 million years ago.

    So, you can see that physical descent of those proteins and neutral variation in them through time is a rather good explanation for the pattern of ks in existing protein coding genes.

    Anyone wants to offer a different explanation?

  145. 145
    ThickPython says:

    @BornAgain77, #139:

    Not to stir up a hornets nest, but,,,

    Vincent Torley Thinks I Have Egg on My Face
    Ann Gauger June 10, 2016

    My quick response:

    https://roohif.wordpress.com/2016/06/11/where-did-that-guy-get-his-data-from/

  146. 146
    Mung says:

    Even the most ardent young earth creationist accepts common descent.

    To the young earth creationists here at UD:

    Pick a group of modern species that you believe is related by common descent. Their ancestors came off the ark along with Noah and his family. They multiplied and diverged.

    What evidence and/or arguments would you offer in favor of your theory of common descent that would be accepted by someone who thinks each species was individually seeded on earth by aliens last Thursday?

  147. 147
    Mung says:

    To the crowd who think common descent deniers are being obstinate.

    How do you determine that a given chromosome is shared between species due to a common ancestor?

  148. 148
    ThickPython says:

    Lastly, I don’t know where Torley’s computer scientist friend Glenn Williamson got his figures, but they do not match the data reported in the paper.

    If the alignment was as high as Williamson said over such a long stretch, surely it would have been reported by the authors. It certainly doesn’t agree with the figures I have shown from the original paper itself.

    There is no other alignment around it, let alone 1500 bases with 73 percent identity. I’ll leave readers to judge whether Williamson’s alignments are valid.

    ELL. OH. ELL.

  149. 149
    bill cole says:

    Gpuccio
    Thanks for this very interesting discussion 🙂

    The first question is what is the mechanism that changed these proteins. I do cancer research and have studied P53 which protects the cell from un wanted cell division. It is a protein that resides in the nucleus and has to interact with many other proteins. This requires both shape and charge fit. It is extremely mutation sensitive since it has to interact with many other nuclear proteins. For a new specie any change in P53 will require change in the other proteins the p53 interacts with. In other words simultaneously changing protein coding gene sequences. I think each specie requires new sequences that have to be right the first time. Yes, Mung, we may be dealing with billions of unexplained origin events 🙂

  150. 150
    ThickPython says:

    @BornAgain77, #125:

    For instance, you ‘ran away’ from this at 24,,,

    In post #24, you posted EIGHT links. In my post #28, I addressed ONE of those – you completely ignored my response and now you want me to address a different point – and yet you reject the label of ‘Gish Galloper’? You’re a textbook example.

    So I’ll ask again – do you still believe that the shark-human-zebrafish article is a problem for common descent? If you think the human being closer to the shark is contradictory to common descent, then I urge you to read my post at #28 again.

    … your preferred mechanism is grossly inadequate for the claims you are placing on it.

    I don’t recall stating a preferred mechanism.

  151. 151
    bornagain77 says:

    Sorry Python, no time to play with trolls who are hypocrites. And anyway, you need to answer Dr. Gauger’s questioning of your methodology instead of trying to be fallacious with me.

  152. 152
    bornagain77 says:

    gp, you go on about sequence similarity as if it proves your point and yet you ignore the fact that similar sequences in unrelated species falsifies your point. Not good science on your part! You can’t just cherry pick what you want and ignore contradictory evidence when you are trying to build a robust case for your position. You must explain ALL the data, not just the parts you pick because it supports your preferred conclusion.

  153. 153
    ThickPython says:

    @BornAgain77, #151:

    And anyway, you need to answer Dr. Gauger’s questioning of your methodology instead of trying to be fallacious with me.

    I posted the alignments on my blog:

    https://roohif.wordpress.com/2016/06/11/where-did-that-guy-get-his-data-from/

    You can verify them for yourself.

  154. 154
    bornagain77 says:

    Thanks Python. You managed a post without a slur.

    Perhaps you can place that link on the lead thread where she might see it?

    And might I suggest you try to be more polite with her than you have been with others who disagree with you?

  155. 155
    wd400 says:

    Bill,

    Gene products react with the environment, of course. But even in this case you are talking about an effect that is mediated by a protein that binds to vitD to do all that transcription.

  156. 156
    Querius says:

    ThickPython @ 122 snorted:

    OH THAT CHALLENGE! I remember now – the one that wasn’t directed at me in the first place, the one that wasn’t in response to any claim that I had made, the one that required me to set up a laboratory at my own expense . . .

    Yeah. It’s called “science,” and many people engage in it to learn more. What’s great about “science” is that it replaces a lot of huffing and puffing with observable results.

    When someone like you or Professor Swamidass makes assertions of common descent through evolution, the burden of proof lies with you, not on the audience to your assertions.

    So. Simply subject some non-motile bacteria to proportionally high levels of ionizing radiation matching an appropriately large number of generations so they can evolve flagella, cilia, legs, propellers, pogo sticks or whatever. You will then conclusively demonstrate common descent for a variety of locomotion genes.

    Imagine the pride and satisfaction you’ll get looking through a microscope at bacteria that have evolved tiny steam engines, proving to everyone that you were totally right!

    Unless you’re afraid you won’t actually get any results. Oh my!

    How about it? And Professor Swamidass, doesn’t this sound like a fun project?

    -Q

  157. 157
    Origenes says:

    Bornagain @152,

    Bornagain: gp, you go on about sequence similarity as if it proves your point and yet you ignore the fact that similar sequences in unrelated species falsifies your point.

    Indeed. Why is it that Venema is not talking about the striking genetic similarities between humans, bananas and/or flies? Is it because our relatedness to the chicken is more plausible?

    Drosophila began to be used to study neurological diseases about 10 years ago when, through the efforts of the Drosophila and human genome projects, it became apparent that the genetic makeup of the fruitfly was surprisingly similar to humans. About 75% of all known human disease genes have fly homologues 1. While the majority of human genes have a fly counterpart, the fly genome is much more “compact” with smaller gene families and less redundancy, fewer and smaller introns and spliced variants, and simpler noncoding regulatory regions, thus making genes easier to study and their functions easier to understand.

    Lloyd & Taylor, 2010

    Overall identity at the nucleotide level or protein sequence between fly and mammal is usually approximately 40% between homologs; however, in conserved functional domains, it can be 80 to 90% or higher.

    Pandey & Nichols, 2011

  158. 158
    gpuccio says:

    bill cole at #149:

    “The first question is what is the mechanism that changed these proteins.”

    I assume that most synonymous mutations (measured by the ks) are mostly neutral (there are many good reasons to believe that), even if some can be deleterious and subjected to negative selection.

    Non symonymous mutations include three possibilities:

    a) Deleterious mutations, which are erased by negative selection (which is the reason why ka is almost always lower than ks).

    b) Neutral mutations, which change the AA sequence, but not the structure and function of the protein (IOWs, those changes which are tolerated by that particular protein).

    c) Possible functional mutations: those are IMO designed, especially if they are complex enough.

    The difficult thing is to distinguish c) from b), because both are measured by the ka. However, ks is much more constant than ka, if we compare the same couple of species. Both ka and ks tend to grow with time separation between species, but ks growth is much more protein independent than ka, and therefore depends more strictly in time. All that is much in accord with the model I have proposed.

    Now, I think that fora protein like myoglobin most changes are probably neutral. Indeed, myoglobin function is probably rather similar in different species, although some functional tweaking of the molecule is certainly possible.

    A molecule like p53 is more likely to have functional mutations which are species specific, given its regulatory function as a transcription factor.

    I hope that answers your points.

  159. 159
    gilthill says:

    Gpuccio,
    Thanks for your nice examples.
    But imagine a model with 3 independant creation events, one for jekko (300 millions years ago), one for mouse (80 million years ago) and one for human (10 000 years ago). Imagine that at their date of creation, these creatures were endowed by their creator with similar p53 and myoglobin genes. Wouldn’t this model fit with the ks and ka data ?

  160. 160
    bornagain77 says:

    Origenes, thanks for the references to fly/human homologs.

    Funny, I don’t feel like a fly. 🙂

    Trailer – The Fly (1986)
    https://www.youtube.com/watch?v=flGCik0MMKo

    Of related interest, and contrary to Darwinian thinking, you can switch these homologs between different species out and still have a normal functioning species.

    Efforts to make and apply humanized yeast – Oct. 13, 2015
    Excerpt: A large proportion of yeast protein-coding genes that have been tested can be replaced with their human orthologs.
    http://bfg.oxfordjournals.org/.....l.pdf+html

    On Human Origins: Is Our Genome Full of Junk DNA? Pt 2. – Richard Sternberg PhD. Evolutionary Biology – podcast
    Excerpt: “Here’s the interesting thing, when you look at the protein coding sequences that you have in your cell what you find is that they are nearly identical to the protein coding sequences of a dog, of a carp, of a fruit fly, of a nematode. They are virtually the same and they are interchangeable. You can knock out a gene that encodes a protein for an inner ear bone in say a mouse. This has been done. And then you can take a protein that is similar to it but from a fruit fly. And fruit flies aren’t vertebrates and they certainly are not mammals., so they don’t have inner ear bones. And you can plug that gene in and guess what happens? The offspring of the mouse will have a perfectly normal inner ear bone. So you can swap out all these files. I mentioning this to you because when you hear about we are 99% similar (to chimps) it is almost all referring to those protein coding regions.
    http://www.discovery.org/multi.....-dna-pt-2/

    What should be needless to say, if you can switch homologs out between very different species and still have a functioning species, then sequence similarity is not telling you anything important about how it is possible to change one kind of creature into another kind of creature.

    “If the overall biology of the animals tells you that they are very different, and the genetics tells you that they are nearly identical, it follows that the genetic comparison is telling you something relatively trivial about the overall biology.”
    Jonathan Marks – evolutionary biologist/anthropologist at the University of North Carolina – 1993
    http://www.evolutionnews.org/2.....89441.html

    Doug Axe, whom, by the way, has a book coming out next month, remarked that what Darwinists, (and apparently Theistic evolutionists), need to concentrate on are the differences that actually can ‘do the trick’ and not on the similarities that clearly did not ‘do the trick’.

    Thou Shalt Not Put Evolutionary Theory to a Test – Douglas Axe – July 18, 2012
    Excerpt: My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that (they think) did the trick, but rather a list of mutations that (actually) can do it. Otherwise they’re in the position of insisting that something is a scientific fact without having the faintest idea how it even could be.”
    Doug Axe PhD.
    http://www.evolutionnews.org/2.....62351.html

    “What needs explanation is the differences, not the similarities.”
    Doug Axe
    http://www.uncommondescent.com.....ian-story/

    “Any transition of form is pure fantasy. There is no demonstration of it.”
    Douglas Axe – co-author of Science & Human Origins – video
    http://www.youtube.com/watch?v=XxMmLakH2LQ

    Here is Dr. Axe’s forthcoming book:

    Undeniable: How Biology Confirms Our Intuition That Life Is Designed.
    http://www.undeniabledesign.com/

  161. 161
    gpuccio says:

    gilthill:

    “Imagine that at their date of creation, these creatures were endowed by their creator with similar p53 and myoglobin genes. Wouldn’t this model fit with the ks and ka data ?”

    I don’t think so. The problem is that my argument for descent is not based on the similarities, as BA and many others seem to believe. It is based on the neutral differences in similar molecules.

    Let’s take myoglobin, for example. As you may have read, in my post #158, I believe that it is very reasonable to assume that the function of myoglobin is rather similar in different species: it is not a regulatory protein, it is a protein whose main function is to bind oxygen and release it when necessary.

    Of course, it is possible that some functional differences between human myoglobin and mouse or jekko myoglobin exist, but in general we observe three similar proteins, with similar function.

    Now, is that an argument for descent? No, that’s not my argument. I agree that those similarities can well be explained by common design too. So, as you say, a designer who “creates” the three species at different moments could simply make the myoglobins similar because of functional constraints of the molecule itself.

    But ka and especially ks do not measure the similarities: they measure the differences.

    And ks, in particular, measures differences which are almost certainly neutral, without any consequence of the protein sequence, structure and function.

    Now, you may have read that even synonymous mutations can have functional effects (usually deleterious effects). That’s true. Some cases are known, where synonymous mutations are a cause of disease. There is nothing really surprising in that, because those mutations, while not changing the AA sequence, can affect other factors, like translational efficiency at the ribosome. So, that is true.

    But it is equally true that most synonymous mutations are functionally neutral: that is certainly the case, because we observe a lot of synonymous mutations in proteins which remain completely functional.

    Just to be clear, in protein coding genes a lot of synonymous mutations happen, while non synonymous mutations are much more rare. Why? Because non synonymous mutations often affect the function , and therefore they are strongly eliminated by negative selection, a very simple process which is certainly true and strong, and has nothing to do with the positive selection imagined by darwinists: negative selection just means that mutations which deeply affect important functions are eliminated because, very simply, the biological being which carries them cannot live normally.

    So, that’s why ka is almost always much lower than ks in almost all functional proteins, and the ka/ks ratio is usually well lower than 1. Synonymous mutations are almost always neutral, while non synonymous mutations can be neutral, but are often deleterious.

    Is that clear?

    Now, let’s go back to our designer who “creates” the three species. And please, consider that I do believe that a designer engineers them, even if in my model he does that by adding information to those beings which already exist (descent) and reusing the information which can be reused as it is.

    Now, if each of the three species is engineered “from scratch” (common design, without descent), then we can explain the similarities as due to functional constraints. We agree on that.

    But the point is: how can we explain the differences, especially the synonymous differences which are certainly mostly neutral?

    IOWs, why should the designer each time change the synonymous sites, while he changes much less the non synonymous sites? And, above all, why should he change those synonymous sites proportionally to the time which has gone by?

    That makes no sense: it is not a scientific explanation, just a form of “fairy tale” to justify some belief, exactly the same error that we, very correctly, attribute to darwinists.

    Very simply, I cannot accept that attitude in science. Neither from darwinists nor from IDists. It is simply wrong.

    The model of descent with designed modifications explains very well what we observe:

    a) It explains the new features which make a new species a new species: they are designed, they are introduces into the new species when it first appears, more or less gradually (that remains to be seen), as new complex information that only a conscious, intelligent, purposeful designer could generate. That is pure ID theory, strong ID theory. It is what I strongly believe, and what I have discussed and defended here for years.

    b) It explains the synonymous variation (ks), which is obviously the result of neutral variation which happens in existing proteins, and is carried on by descent, without affecting the functional information in those proteins. That’s why it’s grossly proportional to time.

    c) It explains the non synonymous variation (ka), which is in part the result of neutral variation in the coding sequence (in the measure that it is tolerated by the functional requirements of that specific protein), and in part the result of functional (and almost certainly designed) modifications which make the protein different in different species, so that it can do different things.

    We can see it more in regulatory proteins, like Transcription Factors, as I have tried to argue many times, because regulation differs in different species. That’s one reason why regulatory proteins can have a ka/ks ratio which is higher than what we observe in non regulatory proteins like myoglobin.

    OK, that’s all for the moment.

  162. 162
    bill cole says:

    Gpuccio

    I hope that answers your points.

    Yes, it does, thanks. 🙂

  163. 163
    bornagain77 says:

    gp,

    “The problem is that my argument for descent is not based on the similarities, as BA and many others seem to believe. It is based on the neutral differences in similar molecules.”

    What should be needless to say to you, comparing supposedly neutral differences in similar molecules is not telling us anything whatsoever as to how it is remotely possible for change to occur.

    By your own definition, you assume the changes are neutral changes, and thus they CANNOT be, by your own definition, the changes that produced the differences period. And thus cannot, by your definition, be construed as knock-down proof for common ancestry no matter how compelling you may personally imagine your neutral argument to be. You are making concrete claims far past your ineffective evidential base. It is simply bad science on your part on par with tea leaf reading!

    Thou Shalt Not Put Evolutionary Theory to a Test – Douglas Axe – July 18, 2012
    Excerpt: McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time. Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (>100 million years).

    My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they’re in the position of insisting that something is a scientific fact without having the faintest idea how it even could be. That’s just not what scientists should be doing.
    Doug Axe PhD.
    http://www.evolutionnews.org/2.....62351.html

    also of note:

    The waiting time problem in a model hominin population – 2015 Sep 17
    John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner
    Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,,
    Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information.
    While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man.
    It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.
    http://www.ncbi.nlm.nih.gov/pm.....MC4573302/

    Moreover, even the preceding paper based on population genetics, which falsified Darwinism, falsely assumed that changes to DNA will affect body plan morphogenesis. That simply is not so. You can mutate DNA ’till the cows come home’ and it still will not help:

    ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body-plan. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’
    Stephen Meyer – Functional Proteins and Information for Body Plans – video
    https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1140536289292636/?type=2&theater

    Moreover, alternative splicing codes are very different between even chimps and humans. Yet new codes are not implemented incrementally but are implemented all at once in a top down fashion.

    Alternative Splicing Codes are Species Specific
    https://docs.google.com/document/d/1UMbNM8V2b7mRzPJt05mlev3UO4SG1bMTV5wkNunezjY/edit

    Alternative splicing codes are part of developmental gene regulatory networks of which ‘flexibility is minimal’.

    A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
    Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
    Eric Davidson – developmental biologist
    http://www.evolutionnews.org/2.....79811.html

    Thus, where Darwinists (and apparently Theistic Evolutionists) most need plasticity in the genome to be viable as a theory, (i.e. developmental Gene Regulatory Networks), is the place where mutations are found to be ‘always catastrophically bad’. Yet, it is exactly in this area of the genome (i.e. regulatory networks) where substantial, ‘orders of magnitude’, differences are found between even the supposedly closely related species of chimps and humans.
    Needless to say, since Darwinian evolution presupposes the unlimited plasticity of organisms, this is the exact opposite finding for what Darwinism would have been predicted for what should have been found in the genome.
    If Darwinian evolution were a normal science that was subject to rigorous testing, instead of the pseudo-science that it is, this finding, by itself, should have been more than enough to falsify neo-Darwinian claims.

  164. 164
    gilthill says:

    gpuccio:

    I agree that the model of descent with designed modifications explains your 3 points, a), b) & c).

    But I think that the model of common design without descent explains these 3 points as well.
    To see this, lets go back to my model of 3 independant creation events, one for jekko (300 millions years ago), one for mouse (80 million years ago) and one for human (10 000 years ago). As soon as these creatures appear on earth, they will be subjected to genetic entropy. As a result, their p53 and myoglobin genes will accumulate mutations, with the number of synonymous mutations being higher than the number of non synonymous mutations for exactly the reasons you mentionned (« Synonymous mutations are almost always neutral, while non synonymous mutations can be neutral, but are often deleterious. »). And the number of mutations (synonymous or not) will be higher in jekko than in mouse because jekko will have been subjected to genetic entropy for a longer time than mouse (300 million years vs 80 million years).
    The bottom line I think is that the Ks argument is unable to decide between the 2 models, common descent with designed modifications vs special creation.

    Until very recently, I was convinced by common descent with designed modifications. But having followed the wonderful works of John Sanford these few last years, I must admit that I am becoming more open to the idea of special creation, at least for man (http://www.logosra.org/#!adam–eve/cde3).

  165. 165
    Querius says:

    Thank you, gilthill.

    http://www.uncommondescent.com.....provement/

    I’m ordering John’s book now!

    -Q

  166. 166
  167. 167
    Eric Anderson says:

    wd400:

    Buy what, if not DNA sequence, controls biological function? I guess you are going to say methylation, transcription factors functional RNA etc, but all of those are encoded by DNA.

    Two points:

    First, it is an open question whether DNA contains all information relevant to an organism. The traditional neo-Darwinian approach certainly holds to this idea (and Matzke has affirmed as much in these pages). However, it is an assumption without proof and there is growing research suggesting that there is significant informational content outside of the DNA.

    Second, even if DNA contains the blueprint for every part and detailed instructions for every process, it still does not mean that DNA “controls” every biological function. I can easily store a complete copy of all the detailed manufacturing specifications for my computer on my hard drive. But that does not mean that my hard drive is “controlling” my computer; nor does it mean that information in my computer exists only on my hard drive; nor does it mean that information flows only one way from my hard drive out and never in.

    The Central Dogma and associated claims have turned out to be not only spectacularly wrong, but a significant hindrance to our understanding of biology. They deserve to be thrown in the trash bin of history, along with the laughable claim underlying the whole enterprise: that a long series of random mistakes to a database can create a new organism.

  168. 168
    gpuccio says:

    BA at #163:

    I really consider you a friend, but I don’t understand why you insist in misunderstanding what I say. Is my English so bad, after all? 🙂

    You say:

    “What should be needless to say to you, comparing supposedly neutral differences in similar molecules is not telling us anything whatsoever as to how it is remotely possible for change to occur.

    “By your own definition, you assume the changes are neutral changes, and thus they CANNOT be, by your own definition, the changes that produced the differences period. And thus cannot, by your definition, be construed as knock-down proof for common ancestry no matter how compelling you may personally imagine your neutral argument to be. You are making concrete claims far past your ineffective evidential base. It is simply bad science on your part on par with tea leaf reading!”

    But I absolutely agree that neutral changes cannot be the changes that produced the differences. As I absolutely agree with what Axe says in the paragraph you quote.

    Can you please quote any statement by me, here or elsewhere, where I say that neutral changes produce functional differences? Or any difference at all? Please, if you can, do it, but if you can’t, just avoid putting concepts in my mouth that I have never expressed.

    I certainly can quote many statements from this same thread where I say just the opposite (IOWs, I say the same thing that you say). This single passage from my post #1 should suffice:

    “To be clear, and to avoid the usual misunderstandings, what I am discussing here is descent with designed modifications, and nothing else. We all agree that all the new complex information which arises in all species is designed, and cannot be explained by any neo-darwinian theory, or more generally by any non design theory which does not imply the explicit intervention, in time and space, of some conscious, intelligent and purposeful being as a designer. Not even a single new complex protein can be explained without a designer.”

    Now, if I say that “not even a single new complex protein can be explained without a designer”, how can you say that I think that neutral variation is the cause of differences?

    However, just to be even more clear:

    a) I think that each new functional protein, functional network, regulatory network, body plan, and so on, IOWs each new function which appears at some time in natural history, is explicitly designed by the explicit addition of new functional information to what already exists. The only requirement is that the function is complex enough to allow a design inference, according to the most standard ID theory. To be even more clear, not even one of these new functions can be explained in terms of common descent.

    b) Instead, the functions which are simply carried on from species to species, without the addition of new information, show the effects of neutral variation, proportional to time, and therefore are evidence of the physical descent of those molecules from species to species.

    This is my argument. I am happy that you think differently, but please don’t make me say things that I have never said.

  169. 169
    gpuccio says:

    gilthill at #164:

    You are the only one here, up to now, who is giving a true counter argument to my argument, based on a good understanding of what I say. I really appreciate that. That’s how a real discussion should be. 🙂

    Your argument is also a good one. It deserves some detailed discussion at different levels. So, I will answer in two or three different posts. I also need a little time to give a thorough answer at all levels. I hope you will be patient!

  170. 170
    bornagain77 says:

    gp, contrary to your claims to the contrary, you are making claims for common descent far past your empirical base. In fact, I think you said something earlier in the thread to the effect that that your reasoning was ‘scientific’ and anyone who disagreed with you, and Torley, was not being reasonable. No matter how you may personally feel about my criticism of your position, it is your reasoning that is not ‘scientific’ in this matter:

    Here is my post on the non-falsifiability of your position on Dr. Gauger’s thread:

    http://www.uncommondescent.com.....ent-610029

  171. 171
    gpuccio says:

    gilthill:

    The first part of my discussion is about your argument. I quote you:

    “But I think that the model of common design without descent explains these 3 points as well.
    To see this, lets go back to my model of 3 independent creation events, one for jekko (300 millions years ago), one for mouse (80 million years ago) and one for human (10 000 years ago). As soon as these creatures appear on earth, they will be subjected to genetic entropy. As a result, their p53 and myoglobin genes will accumulate mutations, with the number of synonymous mutations being higher than the number of non synonymous mutations for exactly the reasons you mentionned (« Synonymous mutations are almost always neutral, while non synonymous mutations can be neutral, but are often deleterious. »). And the number of mutations (synonymous or not) will be higher in jekko than in mouse because jekko will have been subjected to genetic entropy for a longer time than mouse (300 million years vs 80 million years).
    The bottom line I think is that the Ks argument is unable to decide between the 2 models, common descent with designed modifications vs special creation.”

    Now, I want to address your argument at two different levels:

    a) Technical

    b) Epistemological

    IOWs, I will try to show why the argument would not be really a good argument epistemologically, even if it worked at the technical level. Then I will show why the argument does not really work at the technical level.

    But, as a first step, I must clarify better how your argument must be to be able to work as an explanation. IOWs, I will try to detail your argument better. If I am wrong in interpreting your thoughts, I apologize in advance, and I am ready to consider any possible clarification from you.

    So, you argue for a model of special creation of species and common design.

    First of all, I must say that my model is also about “special creation”: the only difference is that I assume special creation of new information which is superimposed on what already exists, while your model assumes special creation of each new being.

    Now, that “special creation”, as far as I can imagine, could happen in two different ways: from nothing (the new being comes into existence “from thin air”), or just “from scratch” (the new being comes into existence from non living matter). I think we can assume, for the moment, the second scenario. IOWs, when the gekko comes into existence for the first time, it is engineered “from the dust” of inorganic, or at least non living, matter. IOWs, each act of “special creation” is a new act of OOL.

    Is that correct?

    In my scenario, instead, the designer generates new information and inputs it into some existing living being. Therefore, while there are huge jumps in functional information (the design acts), there is no jump in descent (each living being comes from an existing living being, at least after the initial OOL).

    OK?

    Now, we must also decide what we consider an act of “special creation”. Each new species? Each new phylum? something in between?

    This point is very important, as we will see.

    In my scenario, the answer is very simple, and I have already given it many times: each time that there is a jump in functional information which is complex enough, I infer a design intervention. I am very strict on that, because that is exactly the consequence of ID theory. Complex functional information, let’s say beyond 100 – 500 bits, requires a design intervention, otherwise it cannot come into existence. As I have said many times, practically each new functional protein superfamily certainly qualifies.

    Therefore, in my scenario, design interventions are very frequent throughout natural history. They are almost the rule.

    But what about your scenario? I see only three possibilities:

    a) “Special creation” acts are rare, for example at the level of OOL and the creation of phyla. The rest follows from natural models, such as neo darwinist evolution. As you can understand, I reject such a possibility on scientific grounds, because each new species has a lot of new functional information, both genetic and epigenetic, which differentiates it even from similar species. That new functional information cannot come from non design sources. Therefore, this scenario cannot work.

    b) “Special creation” acts are rather frequent. Each new species is the result of a special creation act. That is possible, and we will discuss how it applies to the scenario of Ks values.

    c) “Special creation” acts are rare (OOL, phyla), but the following development of species can be explained by design interventions and descent. That is possible, but I reject this scenario because it is really artificial, and definitely not parsimonious. Why invoke two completely different mechanisms (special creation and design interventions) to explain the same kind of problem (complex functional information in living beings)?

    So, in the following discussion, I will go on with the b) scenario:

    – each new species is the result of an act of special creation

    as opposed to my scenario:

    – each new species, indeed each new complex functional protein, is the result of a new act of design on existing living beings.

    OK, that said, your argument can work only if it is in the following form:

    Argument:

    Each new species is the result of an act of special creation. When each new species is created, the proteins and protein genes which simply reuse already existing information (such as myoglobin) are generated “de novo” from non biological matter, according to a common design. The following differences in sequence that we observe, especially the ks, which are grossly proportional to time, can be explained as the effect of neutral variation (or genetic entropy, if you prefer) acting through time. Therefore, more ancient species are changed more than more recent species.

    OK?

    Now, as I see it, that means:

    When a new species is created, it receives a brand new myoglobin gene, which is designed according to a constant common design (allowing for some minor functional tweaking).

    Let’s call this sequence the “gold” gene.

    Of course, that sequence includes both the functionally restricted information (which will not change much, because it is functionally restricted) and the neutral information, including the non synonymous sites. IOWs, there is a “gold” form of the synonymous sites too. That is the part that will change neutrally according to time, explaining the observed pattern of ks.

    So, your argument is that humans, having been created recently, still have the “gold” form of the myoglobin gene, even in the synonymous sites, while gekko, being an older species, has been subject to long years of neutral variation, which explain the high ks when confronted with humans. Mouse is in some way in between.

    OK?

    Now, in next post, I will go on with the technical confutation of this argument, while I will address later the epistemological problems. In the meantime, if you disagree with what I have said up to now, you can certainly intervene.

  172. 172
    gpuccio says:

    BA:

    I had simply asked:

    “Can you please quote any statement by me, here or elsewhere, where I say that neutral changes produce functional differences? Or any difference at all? Please, if you can, do it, but if you can’t, just avoid putting concepts in my mouth that I have never expressed.”

    Can you answer that, please?

    Regarding your link to your post, that is about similarity. As I have said so many times, my argument is not about similarities, but about differences. Again, it is not kind to counter arguments that I have never made as though I had made them.

  173. 173
    gpuccio says:

    BA:

    You say:

    “In fact, I think you said something earlier in the thread to the effect that that your reasoning was ‘scientific’ and anyone who disagreed with you, and Torley, was not being reasonable.”

    What I said is (post #161):

    “IOWs, why should the designer each time change the synonymous sites, while he changes much less the non synonymous sites? And, above all, why should he change those synonymous sites proportionally to the time which has gone by?

    That makes no sense: it is not a scientific explanation, just a form of “fairy tale” to justify some belief, exactly the same error that we, very correctly, attribute to darwinists.

    Very simply, I cannot accept that attitude in science. Neither from darwinists nor from IDists. It is simply wrong.”

    It’s a very different statement from what you “quote”. And I maintain it.

  174. 174
    bornagain77 says:

    This is really getting tedious. gp you state your ‘scientific’ argument as such

    “why should the designer each time change the synonymous sites, while he changes much less the non synonymous sites? And, above all, why should he change those synonymous sites proportionally to the time which has gone by?”

    And as ‘time has gone by’, why in blue blazes are highly similar sequences found in widely divergent species that have supposedly been separated for tens to hundreds of millions of years?

    You simply are not allowing the falsifying evidence to have a place in your reasoning. i.e. you are not being ‘scientific’.

    No hard feelings , but It is really not that hard to understand, and I really don’t feel like explaining that simple point over and over to you.

    again, Here is my post on the non-falsifiability of your position on Dr. Gauger’s thread:
    http://www.uncommondescent.com.....ent-610029

    I’m sure you will disagree again that you are being unreasonable, but I am done trying to explain this simple point to you.

    Have a good day

  175. 175
    gpuccio says:

    gilthill:

    Now, the technical confutation.

    The problem is, it is not true that gekko as a species appeared 300 million years ago. The split which happens about 300 million years ago, according to the fossil record, is the fundamental split between Synapsida (the group which includes mammals, and therefore humans) and Sauropsida/Reptilia (as you prefer), the group which includes lizards. Both groups are part of Amniota, but they differ for many basic features.

    So, according to a descent explanation, we have about 300 million years split between the last common ancestor of lizards and humans.

    But when did really gekko japonicus appear as a species? Well, I am not an expert, but from what I have found it should be about 100 – 80 million years ago.

    The idea is: if we use descent as an explanation, we must look at the last common ancestor before a split. But if we use special creation of individual species, we must look at the time of appearance of that species in the fossil record.

    The point is: most species that we observe today are rather recent, while their ancestors (if we accept the idea of descent) are much older.

    Let’s see how that works for gekko.

    If we accept the idea of descent, then the ks we have found for myoglobin (1.49) is perfectly consistent for a 300 million years gap with the last common ancestor. It is, indeed, almost 2.32 times the value we find for mouse (0.64), which corresponds to a split of about 80 million years.

    But, if we accept your scenario, the gekko was specially created 80 – 100 million years ago. Therefore, if it received its “gold” version of the myoglobin gene, the ks with humans should be much lower, similar to that of mouse. But that is not the case.

    Can we prove that even better? Yes, we can.

    Lizards and snakes are supposed to have split much later than the 300 million years which correspond to the split between Synapsida and Sauropsida. Probably, about 100 million years ago.

    So, I have computed ks values for a snake, Python bivittatus.

    First of all, let’s compare python myoglobin to huamn myoglobin:

    Pythos vs human myoglobin:

    ka = 0.206900 ks = 1.73050 ka/ks = 0.119560

    Let’s compare those values with those of gekko:

    Gekko vs human myoglobin:

    ka = 0.185171 ks = 1.490985 ka/ks = 0.124194

    As you can see, there is a very good correspondence, which is perfectly compatible with the descent scenario: indeed, the last common ancestor of Synapsida and Sauropsida, which lived about 300 million years ago, is the same for lizards, snakes and humans.

    Now, let’s look at the values when we compare myoglobin of gekko and python (a lizard and a snake), which diverged about 100 million years ago:

    Gekko vs python myoglobin:

    ka = 0.116197 ks = 0.587024 ka/ks = 0.197942

    As you can see, the ks value is much lower, and very similar to the human – mouse value (0.64).

    Now, if your scenario were true, why should gekko exhibit a ks of 1.49 vs human myoglobin, and a ks of 0.58 vs python myoglobin?

    When was gekko “specially created”? How much time has gone by since it received its version of “gold” myoglobin gene? How much neutral variation has accumulated on that pristine common design? 0.58 or 1.49?

    OK, that is my confutation. In brief, the ks values are grossly proportional to the time from the last split between the ancestors of present species, and not to the time since present species first appeared. That is perfectly compatible with descent with special creation of new information, but not with “special creation” in the sense you use it.

  176. 176
    gpuccio says:

    BA:

    “And as ‘time has gone by’, why in blue blazes are highly similar sequences found in widely divergent species that have supposedly been separated for tens to hundreds of millions of years?”

    What is the problem? They are functionally restricted. That’s why they are conserved.

    As I have argued many times here, the beta chain of ATP synthase is extremely conserved between E. coli and humans. The simple reason is that it has very high functional specificity, and it cannot change by neutral variation.

    Histone H3 is extremely conserved between fungi and humans. The reason is the same.

    That is the foundation of my argument for design inference for those molecules. An inference which is fully based on the assumption of descent.

  177. 177
    gpuccio says:

    BA:

    However, no hard feelings, and have a good day.

    I agree with you, this is really getting tedious.

  178. 178
    mw says:

    Hi Gilthhill, at #164.
    —————————————–
    I must admit that I am becoming more open to the idea of special creation, at least for man (http://www.logosra.org/#!adam–eve/cde3).
    —————————————–

    The following link may be of interest, not so much because it leans in that direction, but because reasonable scientific arguments are used against common descent. http://restoringtruthministrie.....heets.html

    It should not matter that a Catholic wrote the tear sheets, as creationist Catholics are about as rare has hens teeth, which says something when such a book is written.

    Also, the same author, with a forward from a Protestant biologist wrote a brilliant, IMO, book, now in e-book form, see http://kolbecenter.org/store-2.....y=13115134

    I mention Catholisicm because, to my understanding, the broadminded and courteous Dr Torley is of the persuasion, and may find them of interest.

    There are of course, multitudes of excellent Protestant links dealing with alternative scientific interpretations for available historical evidence for origins.

    One day, I suddenly realised, due to a Protestant scholarly book, origins is chiseled out as part of divine law: it must be true, otherwise the Judaeo-Christian God is seriously flawed.

    When such daylight was realised in me, the scriptures became crystal clear, no fudging needed. Of course, origin in those terms, is an act of pure faith. However, it is not blind faith. Jesus confirmed Sinai, and Sinai proved theologically Genesis. Both meet at the Transfiguration, where Jesus spoke to Moses, whom through the Father, one in essence with, He gave the Ten Commandments to.

    Therfore, true science in God, surely, must lean toward the light that Jesus gave: through Him, creation took six days. The maturing effect of a divine miracle we cannot understand. We may believe Jesus matured water into six jars of best wine instantly. No expert wine tester could tell it’s date of creation.

    Of course, expect plenty scoffing!

    By faith we are saved, not Darwinian degrading science so called; who said:

    —————————————
    “I   will   never   allow   that   because   there   is   a   chasm   between  Man…and   animals   that   man   has   different   origin…Man   in   his  arrogance   thinks   himself   a   great   work.     [W]orthy   the  interposition   of   a   deity,   more   humble   &   I   believe   true   to  consider   him   created   from   animals.     –   Charles   Darwin,  writing  in  his  Private  Notebooks.” (A   Catholic   Assessment   of   Evolution   Theory  Weighing   the   Scientific   Evidence   in   Light   of   Thomistic   Principles    and  Church  Teachings  on  Origins)  
    —————————————  

    How arrogant to think God could create us as God said!!! How blind have we become in the pit of Darwin?

  179. 179
    bornagain77 says:

    gp you really need to read my post on Ann Gauger’s thread so you stop embarrassing yourself like you just did. 🙂

  180. 180
    wd400 says:

    I guess I’m just more interested in biology that have y proclamations and inapt analogies. So, if you have some specifics to back up this let me know.

  181. 181
    gpuccio says:

    gilthill:

    Now, the last aspect, regarding scientific epistemology. So, I will really become completely unpopular here! 🙂

    Let’s assume, for a moment, that your argument is working, and that the technical confutation that I have given in post #175 can be refuted. So, let’s say for a moment that common design and special creation can explain the observed pattern of ks as well as my model of descent with designed modifications. Still, I would not accept your model as best explanation for the observed facts, and I would stick to mine.

    Why? Not just out of obstinacy, as many will certainly argue.

    The point is: I fully reject methodological naturalism (the idea that observed facts can only be explained by “natural” causes). I have explained many times here why methodological naturalism is wrong, dogmatic and anti scientific.

    But…

    But I certainly believe that, if a valid explanation based on known principles is available, and if it explains well observed facts, we have no reason at all to look for different explanations which imply more “philosophical” or “religious” ideas, like “special creation”.

    IOWs, I have nothing against considering “special creation”, or any other possible explanation, for some observed facts, but I would consider that option only if no more conventional and reasonable explanation is available.

    That is exactly the case for complex functional information: no credible explanation which does not imply a conscious intelligent designer is available. Therefore, a designer is the best explanation, even if the nature and features of the designer can remain a problem for many. Why? Because we know, from observed facts and good reasoning, that complex functional information is always the result of a design intervention by some conscious intelligent purposeful being. On the other hand, all the alternative theories which do not include a designer, first of all neo darwinism, can easily be shown to be incapable of explaining anything, and are evidently false.

    But for descent the situation is completely different. There is nothing strange in the idea of a designer who engineers new species by acting on existing species. In an extremely limited way, we already do some biological engineering by acting on living beings, for example bacteria. There is nothing unsatisfying in this explanation. You have admitted that my model explains very well observed facts, including the pattern of ks in different species.

    So, design to implement new information, descent with designed modifications and neutral variation (which is something that we can observe all the time) are more than enough to build a model which explains what has to be explained. There is no need to invoke “special creation”, or at least no scientific need at all. If many have religious reasons to do that, I respect their position, but I cannot share it in a scientific discussion.

  182. 182
    Origenes says:

    Gpuccio: Histone H3 is extremely conserved between fungi and humans. The reason is the same.

    That is the foundation of my argument for design inference for those molecules. An inference which is fully based on the assumption of descent.

    Gpuccio, your argument for design, as presented by you e.g. here and here, still stands. It shows convincingly that de novo functional sequences in different groups of organisms cannot be explained by evolutionary theory. However I regard this as an argument against evolutionary theory, not as an argument for descent with designed modifications.

  183. 183
    gpuccio says:

    Origenes:

    It is not an argument for descent. It is an argument for ID based in part on the assumption of common descent.

    The point is: my measurements of the functional information in proteins are based on the bit score you get from blast comparisons,that is on sequence conservation through long spans of time.

    That bit score is a measurement of functional constraints in the sequence because I assume, like all biologists do, that otherwise the sequence would have changed by neutral variation. That is true only if we assume CD. That’s why I compare the human sequence to sequences in other species. That’s why darwinists cannot really object to my reasoning about functionality of conserved sequences: they should deny their own principles.

    That is also the reasoning used by Durston in his famous paper: he measures function from conservation through species. That assumes CD and neutral variation.

  184. 184
    gilthill says:

    Gpuccio, at # 175

    I quote you “Now, if your scenario were true, why should gekko exhibit a ks of 1.49 vs human myoglobin, and a ks of 0.58 vs python myoglobin?”

    Well, I have been unable to find a good answer to this question yet.

    So, at first sight, it seems that the common descent with designed modifications better explains the data you have offered than special creation.

    Also, I thank you for all the very interesting developments you have offered on the topic. It was a pleasure to read you.

  185. 185
    gpuccio says:

    gilthill:

    Thank you. I appreciate your attention and honesty. I remain available for any further discussion on this topic.

    I am also greatful that your comments helped and stimulated me to develop some more in depth analysis.

  186. 186
    Eric Anderson says:

    gilthill and gpuccio:

    Fun exchange and good things to think about.

    Now let’s take it from the theoretical to the practical:

    Given the large number of changes required to turn, say, an ape-like creature into a human, how does this “common descent with designed modifications” get implemented in practice, in the real world? And how would we distinguish that from “special creation”?

    I rarely use the term “special creation” because I’m not sure what it means. Does it mean designed completely de novo, from the ground up? Or does it mean taking an existing system and modifying it? Does it mean even a limited instance of design intervention where purely natural processes cannot fully account for the system in question?

    When dealing with something like the ape-to-human transition, it seems we are dealing with a significant amount of intelligent intervention and additional design work. What does “common descent with designed modifications” look like in practice as it is being implemented, versus “special creation”?

  187. 187
    mw says:

    Prof. S. Joshua Swamidass writes:
    ———————–
    “Once again, if we reject common descent, why do we have this broken gene? What design principle explains this pattern?”
    ———————–

    Perhaps, weakness of common descent explanatory power; or a system that is decreasing/corrupting, not in accordance with the original parameter an intelligent designer set.
    Ref Prof John Sanford: “Critic ignores reality of Genetic Entropy,” http://creation.com/genetic-entropy

    And of course, the contributions of Dionisio:
    http://www.uncommondescent.com.....ent-609671.

    Not forgetting BA77, (of whom Professor Swamidass just gave a ‘glowing’ report!) and others; strongly suggests that we simply do not understand the complex complexity of a single cell, never mind find its place in a framework of interrelated designs, by selective chance and mutation, wrought in common descent.

    The possibility exists, in terms of the spirit, that spiritual weakness, the sins of the father’s (from Adam and according to the clear teaching of Paul), may affect any physical unit or component in a life form, and hence death.

    However, the Professor appears to cast out one divine law; that Christ, one with the Father, wrote and spoke to Moses at Sinai, that He created in six days, according to truthful records; as one would expect.

    We cannot salt Darwinism with Christ and cast out divine law to suit beguiling science. Do Christians expect any Darwinian credibility to stand square, face to face with Christ?

    Biologically speaking, if we do not understand a cell’s true beginning, how can we fully know what will break such a cell? And, which appear in terms of belief, to be related to spiritual law interactions with the physical.

    Prof Swamidass, @ 62, says:

    —————————
    “I’ve been studying (without regard to evolution) for YEARS.”
    —————————

    I believe much of operational science proceeds without regard to Darwinism. It appears, Darwinian science, so called, has invented nothing by following its main axioms dealing with common descent. No wonder people have been studying for years “without regard to evolution.”

    However, again, how many biological scientists and similar, probably would not dare, or not want to, disassociate themselves from the theory and be able to remain in their post in these present times?

    Evolutionists believe we ascend by natural selective descent into perfect designed animals, fit for Darwinian purpose. The theory cannot lose because it has the answer, it believes, to every objection.

    Prof Swamidass also says:

    ——————————
    “I hope some of you take interest in biology for biology’s sake.”
    ——————————
    Well, as Christians; if only we would take an interest in divine law for the sake of Christ, being that Christ died under that law, as “the truth,” and yes, to save us from Darwinism.

    Instead, too may Judaeo-Christians look down the looking glass of the ‘black hole’ of unprovable common descent; be it by PE or by other suggestions, but never ever seeing how, in imperceptible steps, as said before, a possum cells arose from a none possum cells, and before that, none possum cells from dead, lifeless, sterile dust.

    At least in terms of divine law, from Sinai onwards, a historic event was witnessed and recorded, and an unbroken link, never missing, flowed from a miraculous event. No recorded event of opossum transitional forms has been observed operational in real time reality throughout history. Nor reproducible now.

    However, we are where we are at today. The link back to Sinai, embedded in a spiritual belief, has almost disintegrated, due to the all-seeing eye of Darwin, who said God was “erroneous,” and Judaeo-Christianity with its Sinai morality/divine law, crowned with divine love also as divine law; ‘bunkum.’ Why should Christians believe in divine love as law, when casting out another to suit Darwin and not Christ?

    How can any paid up member of Christianity, (through the crucifixion that is), believe such and take sides with such; opposing divine law: no matter how impossible it may seem?

    It may be believed, at Sinai, God intellectually spoke to intellectual creatures with a pattern of sound clear words. Elasticating the word of God beyond recognition to suit Darwin is a grave and scientific error in terms of Judaeo-Christianity divinely revealed, recorded as such by ‘expert’ eye witnesses, having experienced the impossible.

    Judaeo-Christians have a credibility issue because, it is Christians who trample the name of Christ underfoot for Darwin who denied Christ as divine!

    Therefore, “What design principle explains this pattern?” Surely the Ten Commandments pointing back to Genesis explains the pattern?

  188. 188
    Dionisio says:

    gilthill @184

    What do you mean by “special creation”?
    Thank you.

    BTW, just realized that the above question is very related to Eric Anderson’s comments @186
    Perhaps your response to EA will respond my question.

  189. 189
    Dionisio says:

    Eric Anderson and gpuccio

    Since you both have used the term “special creation” in your interesting discussion with gilthill, would you mind saying what did you individually mean by that term in the context where you used it?
    Thank you.

  190. 190
    gilthill says:

    Dionisio @ 188

    In my exchanges with gpuccio, special creation is the idea that complex living things did not descend from simpler ones but were created independently.

  191. 191
    gpuccio says:

    Eric, Dionisio and gilthill:

    gilthill’s answer at #190 is perfectly correct. I will try, however, to elaborate a little more in detail.

    With your permission, I will avoid the example of ape-human transition, because it evokes IMO stronger emotional reactions. After all, we are interested in the general process of species evolution.

    So, let’s look to one of the examples in our discussion: gekkos and pythons.

    We know form the fossil record that sauropsida, or reptiles if you prefer, appear about 300 million years ago, maybe something more.

    Lizards and snakes, instead, appear later as different groups of reptiles. let’s say 100 million years ago. Now, there are many different species of lizards and snakes, but for the sake of argument let’s say that both gekko japonicus and python bivittatus, the two species for which I have computed myoglobin ks, appeared, more or less as they are now, about 100 million years ago.

    So, what have we before that time? We have other forms of reptiles, probably now extinct, I really don’t know. Then, at some time, jekko and python appear.

    Let’s concentrate on gekko. Smaller, friendlier! 🙂

    So, what happens in the two different scenarios?

    I suggest that those really interested in this topic read my post #171 to gilthill. However, I quote here the most pertinent statement:

    “So, you argue for a model of special creation of species and common design.

    First of all, I must say that my model is also about “special creation”: the only difference is that I assume special creation of new information which is superimposed on what already exists, while your model assumes special creation of each new being.

    Now, that “special creation”, as far as I can imagine, could happen in two different ways: from nothing (the new being comes into existence “from thin air”), or just “from scratch” (the new being comes into existence from non living matter). I think we can assume, for the moment, the second scenario. IOWs, when the gekko comes into existence for the first time, it is engineered “from the dust” of inorganic, or at least non living, matter. IOWs, each act of “special creation” is a new act of OOL.”

    IOWs, let’s look at it more in detail, as suggested by Eric.

    Scenario 1: “Special creation of the gekko”

    Let’s call the putative ancestor of lizards and pythons “Reptile X”. Well, in this scenario, Reptile X exists 100 million years ago before the appearance of gekko, but it has absolutely nothing to do with that appearance. What happens is that at some time gekko appears together with Reptile X.

    How? There are two possibilities: it is created from nothing (a true physical miracle); or it is engineered from scratch from non living matter (IOW, a special OOL event, in this case Origin of gekko life).

    All the proteins which are common between Reptile X and gekko are built again from scratch, and they have no physical continuity with the similar proteins in Reptile X. The similarities and differences are to be explained by common design.

    OK?

    The same happens for pythons, and for each new species in natural history.

    OK?

    Now:

    Scenario 2: “Special creation of the new information to get the new species gekko, by descent with designed modifications”

    This is my model. We are again in the previous situation: 100 million years ago, Reptile X exists, gekko is not there yet.

    Some designer, unsatisfied with Reptile X, desires to have a new species, gekko, with new functions and features.

    He intervenes on Reptile X, engineering the new information. The process happens in living Reptile X beings, and in the process those beings go on reproducing. In the process, all the information which needs not be changed is conserved. The new information is added by biological engineering tools, like guided mutations or guided transposon activity, or any other procedure. At some point, the reproducing being is no more Reptile X, but it is gekko.

    Please note the following important points:

    a) The process, in principle, can take any different span of time: it can be instantaneous, or require a few days, or a few years, or a few million years. I have no idea. Only facts can answer that question. I tend to think that the process requires some time, but not too much.

    b) During the process, there is a continuity of reproduction, and a physical continuity. IOWs, the myoglobin gene that we find in the gekko in the end is physically the same that was in Reptile X at the beginning (obviously, through the usual process of DNA replication in cell duplications). The new sequences, instead, are new, engineered from some pre-existing sequence in Reptile X, or in some other way. Guided transposon activity is my best bet as the most common engineering procedure, but many different procedures can be used in the process.

    c) The engineering process happens only in a subset of Reptile X beings: one clone, or a few clones. IOWs, Reptile X goes on with its history. Maybe it becomes extinct. maybe we still have it here today. The new species is derived from a subset of the old species, through an engineering process. The old species remains there.

    d) Of course, once the new species is there, the usual automatic processes of population selection can take place. IOWs, the designer just sets the new species in motions. Each new species, once engineered, enters the “game” of life, and we can assume that no new design interventions are necessary for that particular species, unless at some point it is chosen as the ancestor of some new species, in which case the process is repeated again.

    OK, that’s a rather detailed model, for the sake of discussion. I hope it asnwers Eric’s and Dionisio’s requests.

  192. 192
    vjtorley says:

    Hi gpuccio,

    I’d just like to thank you for posts #181 and 191 above, which state the scientific case for common descent very simply, clearly and elegantly. Thank you once again.

  193. 193
    Dionisio says:

    gilthill @190

    In my exchanges with gpuccio, special creation is the idea that complex living things did not descend from simpler ones but were created independently .

    were created independently ?

    How?

    Is that what gpuccio@191 calls “from scratch” just using the raw material, not cells?

    Could that be through “designed modifications” applied to a previous ‘version’ as per gpuccio@191, kind of like what Venter and his folks do?

    Do you adhere to the excellent detailed model provided by gpuccio@191?

  194. 194
    Dionisio says:

    gpuccio@191

    Thank you for the clear detailed model you have described, as usual. I’ve learned quite a bit from what you’ve written in this site and look forward to learning more.

    I have a couple of questions, but they might be dumb in the sense that either don’t make biological sense or that you have answered them already @191 or before in this thread.
    However, since you have dealt so politely even with trolls in this forum, I know you will treat me nicely because you know my questions (including the dumb ones) are intended for learning, not trolling. BTW, a few weeks ago I toured some Norwegian fjords and saw a bunch of real trolls everywhere, but they were much nicer than some of the trolls we have seen here. 🙂

    I understood the example you provided is about comparing myoglobin between gekko japonicus and python bivittatus, which are two different species of reptiles, which allegedly descend from a common reptile ancestor X. Did I get this right?

    Are there other differences between the gekko and the python besides the myoglobin?

    Were the designed modifications made in the development process of reptile X in order to make the development process of the gekko and the python or the myoglobin differences were post-developmental?

    Did the changes made in the development process of reptile X only affect the myoglobin or also affected other proteins?

    Did the introduced changes affect the DNA sequences associated with myoglobin or also affected epigenetic markers and/or feedback/feedforward loops in regulatory networks, signaling pathways, oscillator impulses (amplitude, period), proto-mRNA splicing mechanisms, post-translational modifications, folding chaperones, etc. ?

    Did the changes made in the development process of reptile X follow a given spatiotemporal sequence in order to make the development process of the gekko and the python separately?

    Could it be that the python development process was made from modifications to the gekko development process or vice versa?

  195. 195
    Eric Anderson says:

    VJT @192:

    . . . which state the scientific case for common descent very simply, clearly and elegantly.

    gpuccio has done a good job of trying to lay out how significant, purposeful, designed intervention can occur to create a new species. And because there is some continuity of reproduction (we can still press on this quite a bit more, which I may do in a later comment, but we’ll leave it for now), then there is a use of the words “common descent.”

    Fine. Fair enough.

    And do you acknowledge that this kind of “common descent” is radically, fundamentally different from the “common descent” that evolutionary biologists, evolution textbooks, and standard evolutionary sources are proposing?

    I’m hoping you recognize this, but just want to make sure we are on the same page.

  196. 196
    gpuccio says:

    VJ:

    Thank you. I am grateful for your kind words. 🙂

  197. 197
    gilthill says:

    Maybe in the grand sheme of life, some specialized organisms in the past have fonctionned somewhat as stem cells in the development of individual organisms, giving rise to many different more differentiated organisms. And maybe it is these specialized “stem organisms” that were specially created.

  198. 198
    gpuccio says:

    Dionisio:

    Thank you. You are always a friend!

    As usual, your comments give me a precious occasion for some clarifications.

    “I understood the example you provided is about comparing myoglobin between gekko japonicus and python bivittatus, which are two different species of reptiles, which allegedly descend from a common reptile ancestor X. Did I get this right?”

    Yes. Indeed, I am no expert of fossil records and related phylogenies, so I have really no idea of what the common ancestor of lizards and snakes could be. That’s why I called it “Reptile X”, just for my discussion. However, it seems quite correct that reptiles appear about 300 million years ago, while the specific groups of lizards and snakes are about 100 million years old.

    “Are there other differences between the gekko and the python besides the myoglobin?”

    Of course. A lot of them, I suppose.

    “Were the designed modifications made in the development process of reptile X in order to make the development process of the gekko and the python or the myoglobin differences were post-developmental?”

    Well, I have chosen myoglobin exactly because I think that it is a protein whose structure and function remain rather stable in vertebrates. Of course, some functional tweaking from species to species probably happens, but I think we can assume that the molecule needs no major engineering from species to species, and is passed on mainly passively. IOWs, it is probably not the object of new design in these transitions (of course, the molecule itself was designed in the beginning).

    So, I assume that the modifications of myoglobin in vertebrates are mainly neutral, and not the result of design. IOWs, both the synonymous differences measured by the ks and the non synonymous differences measured by the ka are simply the result of neutral variation, in the species we have considered.

    So, what happens? Let’s consider just the values of ks, which are almost certainly the expression of neutral variation.

    I have considered two different cases:

    a) gekko and humans. In this case, the last common ancestor can be grossly assigned to 300 million years ago, when amniota become splitted into sauropsida (ancestors of reptiles) and synapsida (ancestors of mammals). The two lines diverge at that time, and they receive from the common ancestor the same myoglobin gene.

    So, when we compare the gene from gekko with the gene from humans, both genes have been exposed, each in its line, to about 300 million years of neutral variation in its synonymous sites. The measure ks for that comparison is 1.49.

    Second case: jekko and python. Here, the split is about 100 million years ago. At that time, the two new lineages receive the same gene from the common ancestor, the fancy Reptile X. Of course, that gene has already been changing neutrally for about 200 million years from the time of the previous split (sauropsida and synapsida). But the copy that lizards and pythons receive at the beginning of their diverging history is more or less the same: the gene as it is in Reptile X at that time (100 million years ago).

    From that moment, that version of the gene changes for neutral variation in each lineage for about 100 million years. When we compare the myoglobin in gekko with the myoglobin in python, today, we find a ks value of 0.587.

    The idea is, the ks value we measure in different comparisons corresponds more or less to 0.5 per 100 million years, obviously with some variance.

    IOWs, protein coding genes change in lineages which split at some definite time so that the measured ks, when we compare gene sequences today, is about 0.5 synonymous substitutions per synonymous site per 100 million years.

    You can find a similar estimate of that value for other proteins here:

    http://darwin.eeb.uconn.edu/ee.....node3.html

    where the value is expressed per billion years, and is something less than 5.

    “Did the changes made in the development process of reptile X only affect the myoglobin or also affected other proteins?”

    If we accept my assumption that myoglobin is mostly non engineered in the transitions we have considered, then it is obvious that the designed changes, those that make a gekko so different from a snake, must happen in other proteins, and in non coding sequences. IOWs, mainly in regulatory sequences.

    “Did the introduced changes affect the DNA sequences associated with myoglobin or also affected epigenetic markers and/or feedback/feedforward loops in regulatory networks, signaling pathways, oscillator impulses (amplitude, period), proto-mRNA splicing mechanisms, post-translational modifications, folding chaperones, etc. ?”

    See previous point. I think that at this level (vertebrate evolution) the changes are mainly in epigenetic regulators, IOWs non coding sequences. But of course, also important regulatory proteins, like transcription factors (for example p53) must change in some measure to implement the functional differences.

    “Did the changes made in the development process of reptile X follow a given spatiotemporal sequence in order to make the development process of the gekko and the python separately?

    Could it be that the python development process was made from modifications to the gekko development process or vice versa?”

    Well, I don’t know. I have accepted in my discussion the idea that lizards and snakes diverge about 100 million years ago, which seems to be a reasonable hypothesis according to what we know. Again, I am no expert of the fossil record and derived phylogenies. I just needed some real example to apply my measurements and my reasonings.

  199. 199
    gpuccio says:

    gilthill:

    I am certainly open to that possibility. I have always said that I think there is a lot of evidence in favor of CD, or more correctly of descent with designed modifications. But I have also said, many times, that CD needs not be universal.

    My only point is: whatever the answer, it must come from facts. I am very confident that many new facts will be discovered in time, and that many more accurate scientific answers will be found.

    Of course, getting rid as soon as possible of unscientific dogmas like neo-darwinist ideology would certainly help! 🙂

  200. 200
    Dionisio says:

    gilthill @197

    I would rather try to understand gpuccio’s model in all its dimensions, because it’s based on rational conclusions derived from the available data. However, due in part to my poor biology background, it’s not easy for me to understand how it works in a wider context. That’s why I asked a few basic (sometimes dumb?) questions @194.
    Definitely this seems like a very enlightening discussion.
    I’d encourage everyone here to carefully analyze the model gpuccio has described so clearly in this thread and put to test every single concept that is presented within it.
    We all could learn from this exercise, though perhaps I’m learning the most. 🙂

    PS. after posting this comment, I noticed gpuccio had written a lengthy comment in reference to 194. I’m going to read it now.

  201. 201
    Dionisio says:

    gpuccio @198

    thank you again for answering my questions. As usual, I have to slowly “digest” your detailed explanation in order to understand it well, but from the first reading it seems like you have clarified a few issues that I had not understood before.

  202. 202
    Dionisio says:

    gpuccio @198

    If we accept my assumption that myoglobin is mostly non engineered in the transitions we have considered, then it is obvious that the designed changes, those that make a gekko so different from a snake, must happen in other proteins, and in non coding sequences. IOWs, mainly in regulatory sequences.

    I think that at this level (vertebrate evolution) the changes are mainly in epigenetic regulators, IOWs non coding sequences. But of course, also important regulatory proteins, like transcription factors (for example p53) must change in some measure to implement the functional differences.

    Are those “designed” changes in the Reptile X regulatory sequences or epigenetic markers (or anywhere else) –that lead to the modification of the Reptile X development process in order to produce the gekko development process– documented and explained as far as you know?
    If not for the reptiles then for another class of biological systems that could be presented similarly as a common ancestor followed by its descendants?

  203. 203
    Dionisio says:

    gpuccio,

    #202 follow-up

    Since the development process of the gekko can be compared with the python development process, thus seeing the differences in gastrulation, neurulation, other portions of the embryonic development, etc., the common portions of the two processes could be understood as conserved from their common ancestor, but the portions of the process that don’t match contains the differences that have to be accounted for to figure out the possible mechanisms that could have produced such process changes. That seems like the type of work they describe in the evodevo literature. Have you seen it too? Does your model cover that too?

  204. 204
    Dionisio says:

    gpuccio

    #203 follow-up

    Instead of the gekko and the snake, could we use the cat and the dog?
    Their development processes are most probably better known and described in details, hence we could see what’s common and what’s not.

  205. 205
    Dionisio says:

    gpuccio

    Ok, I understand that your example calculating and comparing ks and ka for myoglobin in gekko and python relative to their common reptile ancestor and even to humans shows the effects of functional conservation and neutral variations. Did I get this right now?
    If not, please indicate the error. Thank you.

    Could the same type of calculations/comparisons help to detect/identify novel designed molecules or parts? Was that what you explained in a previous thread with an impresive shark picture, where you included a graph with a blue part that corresponded to “de novo” information?

  206. 206
    Dionisio says:

    gpuccio

    If we denote the ancestor reptile X development process as Dev0 while the development processes for the gekko and python could be labeled Devg and Devp respectively, can we say that
    Devg = Dev0 + Deltag
    Devp = Dev0 + Deltap

    Where Deltag and Deltap are the whole set of specific changes made in Dev0 in order to have Devg and Devp respectively ?

    Does this make sense?

  207. 207
    Dionisio says:

    gpuccio

    #206 follow-up

    If that definition is valid (acceptable), then does your CD model include or cover the study of Deltag and Deltap too?

    I think I have seen some examples of that in recent evo-devo papers. Do you recall seeing it too?

  208. 208
    Dionisio says:

    gpuccio,

    #207 follow-up

    What would you suggest to do in order to make an accurate comprehensive spatiotemporal description of the sequence of events associated with Deltag and Deltap ?

  209. 209
    Dionisio says:

    gpuccio

    FYI, the last seven posts @202-208 are related to some of the issues that have hindered the progress of one of the projects I’ve been working on lately.
    I’ve been gathering information mostly from sources outside this site, but your insightful comments are highly appreciated too.

  210. 210
    gpuccio says:

    Dionisio:

    I apologize for coming back so late, I was really busy.

    But… Wow! How many questions! 🙂

    OK, let’s start.

    #202:

    “Are those “designed” changes in the Reptile X regulatory sequences or epigenetic markers (or anywhere else) –that lead to the modification of the Reptile X development process in order to produce the gekko development process– documented and explained as far as you know?
    If not for the reptiles then for another class of biological systems that could be presented similarly as a common ancestor followed by its descendants?”

    Yes. I think that designed changes, mainly in the regulatory networks, are what change the developmental procedures and make a species what it is. Of course, effector proteins too change, or new proteins appear de novo. That too, obviously, is designed change. But in the most recent phase of natural history (let’s say development inside already formed phyla) change is probably mostly regulatory.

    #203:

    “Since the development process of the gekko can be compared with the python development process, thus seeing the differences in gastrulation, neurulation, other portions of the embryonic development, etc., the common portions of the two processes could be understood as conserved from their common ancestor, but the portions of the process that don’t match contains the differences that have to be accounted for to figure out the possible mechanisms that could have produced such process changes. That seems like the type of work they describe in the evodevo literature. Have you seen it too? Does your model cover that too?”

    I think you are right. Many key epigenetic regulators are active during embryonic development. The problem is hat we still understand too little. Evodevo is an interesting approach, provided it is not completely conditioned by the neo darwinian ideology.

    #204:

    “Instead of the gekko and the snake, could we use the cat and the dog?
    Their development processes are most probably better known and described in details, hence we could see what’s common and what’s not.”

    We can look at any kind of similar species, but anyway we still understand too little.

    And we must be prepared to meet interesting paradoxes. Just two extreme examples:

    a) C. elegans and C. briggsae. Two small worms. About 100 million years of separation. The genomes have many similarities, but a lot of differences too. From the “wormbook”:

    “C. briggsae has about 800 genes that have not be found in C. elegans, while C. elegans has 1,061 genes that have not been found in C. briggsae”

    Well, is that interesting? Yes, it is, because the amazing facts is that the two worms are extremely similar morphologically and phenotypically.

    b) The well known case: humans and chimps. Short separation, and small differences in the genomes. And yet: perhaps the biggest functional difference we can imagine between species, if we consider just the complexity of the human brain and its achievements.

    OK, just to motivate my statement: we still understand too little.

  211. 211
    Dionisio says:

    gpuccio
    Caro dottore, your apologies are accepted.
    However, please note that there’s no time deadline associated with my questions. Specially in your case.

    You may choose when to answer them at your own convenience, on your spare time, if you find any and you wish to.
    I have no rights whatsoever to expect that my questions get answered within any time interval, if at all.

    BTW, thank you for responding them! I highly appreciate the time you take to explain things here.

    FYI – I’m learning quite a bit from this interesting discussion. Perhaps this will take care of some of the hurdles that were hindering the progress of a project I’ve been working on lately.

  212. 212
    Dionisio says:

    gpuccio @210

    The well known case: humans and chimps. Short separation, and small differences in the genomes. And yet: perhaps the biggest functional difference we can imagine between species, if we consider just the complexity of the human brain and its achievements.

    Excellent observation. Good point.
    That’s most probably a case where thorough comparative research of the respective development processes (initial cleavage, gastrulation, neurulation, etc.) should help to understand many of the things we still don’t. Is this correct?

    Let’s keep an eye on the papers on this subject that keep coming out of the wet and dry labs everywhere.

  213. 213
    gpuccio says:

    Dionisio:

    #205:

    “Ok, I understand that your example calculating and comparing ks and ka for myoglobin in gekko and python relative to their common reptile ancestor and even to humans shows the effects of functional conservation and neutral variations. Did I get this right now?
    If not, please indicate the error. Thank you.”

    Yes, you got it right.

    “Could the same type of calculations/comparisons help to detect/identify novel designed molecules or parts? Was that what you explained in a previous thread with an impresive shark picture, where you included a graph with a blue part that corresponded to “de novo” information?”

    Yes, the idea is correct, but there are limitations in the ise of the ka/ks measure. For example, I have computed ka and ks for the prickle protein between human and drosophila, but:

    a) I could only di that for the part of the molecule which can be aligned. As you may remember, while the red part shows a good homology in those two species (bit score 462), the rest of the molecule is completely different. In that case, you cannot align the sequences, and you cannot compute ka and ks.

    For the aligned part (the “red sequence”) I got a ka of 0.33, while the ks cannot be computed because it reaches saturation: that means that there are so many differences between the synonymous sites in the two sequences that those parts are as different as any two random sequences. In that case, my software returns a “symbolic” value of 9.999999 for the ks.

    However, it is obvious that with a ka of 0.33 and a ks so great that it cannot be computed with precision, the ka/ks is certainly very low. That means that this part of the molecule is strongly conserved, even between two so distant species.

    The rest of the two molecules is completely different, so it cannot be compared. And I have shown that this completely different sequences are conserved in their respective lineages: the “blue” sequence is highly conserved in vertebrates, while I have computed ka/ks for the blue sequence in hymenoptera (in my second OP on that subject), with the following results:

    Wasp – Bee: Ka/Ks ratio = 0.09291813

    Wasp – Ant: Ka/Ks ratio = 0.05965076

    Bee – Ant: Ka/Ks ratio = 0.01145057

    IOWs, the “blue” sequence in hymenoptera, while being completely different from the “blue” sequence in vertebrates, is as much conserved in its respective lineage. IOWs, new functional information, lineage specific, which is generated in each lineage to cooperate with the conserved “red” part of the molecule.

    IOWs, great modular design! 🙂

  214. 214
    gpuccio says:

    Dionisio:

    #206:

    “If we denote the ancestor reptile X development process as Dev0 while the development processes for the gekko and python could be labeled Devg and Devp respectively, can we say that
    Devg = Dev0 + Deltag
    Devp = Dev0 + Deltap

    Where Deltag and Deltap are the whole set of specific changes made in Dev0 in order to have Devg and Devp respectively ?

    Does this make sense?”

    Yes, definitely.

    #207:

    “If that definition is valid (acceptable), then does your CD model include or cover the study of Deltag and Deltap too?

    I think I have seen some examples of that in recent evo-devo papers. Do you recall seeing it too?”

    Well, I don’t really know. We need molecular details to analyze those processes from my point of view. MAybe you can point to some examples, and we can see…

    “What would you suggest to do in order to make an accurate comprehensive spatiotemporal description of the sequence of events associated with Deltag and Deltap ?”

    Again, it depends on how much we understand at molecular level. My impression is that the gap between molecular data and morphological/functional data is still huge (unfortunately)!

  215. 215
    mw says:

    A further response by Dr Ann Gauger.

    http://www.evolutionnews.org/2.....02922.html

  216. 216
    vjtorley says:

    Eric Anderson,

    I’d like to answer your question. You write:

    gpuccio has done a good job of trying to lay out how significant, purposeful, designed intervention can occur to create a new species. And because there is some continuity of reproduction (we can still press on this quite a bit more, which I may do in a later comment, but we’ll leave it for now), then there is a use of the words “common descent.”

    Fine. Fair enough.

    And do you acknowledge that this kind of “common descent” is radically, fundamentally different from the “common descent” that evolutionary biologists, evolution textbooks, and standard evolutionary sources are proposing?

    I’m hoping you recognize this, but just want to make sure we are on the same page.

    Short answer before I retire for the evening: Yes, I do.

  217. 217
    Dionisio says:

    gpuccio @210, 213, 214.

    Thank you for your insightful comments, again.

  218. 218
    Dionisio says:

    gpuccio

    Regarding our brief but clarifying (at least to me) discussion, which can be summarized (so far) in your comments @210, 213, 214, and considering that our chat has taken place within a discussion thread started by vjtorley and mainly focused on a debate where Ann Gauger, Joshua Swamidass, Jeffrey Tomkins and Dennis Venema have been named, would it help to invite them all to comment on those posts 210, 213, 214? Perhaps they could shed some additional light on the subject? Just a thought.

    BTW, regarding the main discussion in this thread, which is above my pay grade, apparently it was triggered by someone posting inaccurate comments on a controversial subject. Later that person “kind of” recognized the mistake. This reminds me (again) that one should approach difficult problems with humility, expecting to learn something new every time.

    At this point I would like to refer to the comments posted @2-4 in this other thread:

    http://www.uncommondescent.com.....ent-610446

    and ask whether you see any relation between what is said in those comments @2-4 and what is written @210, 213, 214 here in this current thread.

    From my perspective of very poor biological knowledge, which makes my opinions practically irrelevant, I see a problem with the sometimes apparently “excessive” reliance on quantification methods that can’t answer important biological questions, as illustrated by your comments @210, 213, 214. I recall you’ve been trying to gather information on what you used to call “procedures” in biology a while ago. That’s a humbling task indeed. I look forward to reading your posts on that fascinating topic, someday. 🙂

    Just thinking out loud, knowing that you’re very respectful and careful when interpreting what others write here.

  219. 219
    Dionisio says:

    gpuccio

    Can you calculate ka and ks for the Izumo1 protein between related species to see how much it has changed?
    Thank you.

  220. 220
    Alicia Cartelli says:

    “So, I assume that the modifications of myoglobin in vertebrates are mainly neutral, and not the result of design.”

    Ah, so now things are “designed” or not whenever it’s convenient for us and our “science.”

    It’s like watching a dog chase its tail.

  221. 221
    mike1962 says:

    Alicia,

    Are you an idiot, or do you just play one on TV?

  222. 222
    Mung says:

    It’s like a dog returning to its vomit.

  223. 223
    Dionisio says:

    mike1962 @221

    Trolls are not idiots. Saw many of them in Norway a few weeks ago. Since Norwegians have WiFi access even in the mountains by the fjords, perhaps some of the trolls have found some electronic gadgets left by tourists and have figured out how to get connected and do their trolling thing online too?
    They look kind of funny, tourists take pictures of them, but the locals who got used to their ugliness simply ignored them completely.
    You may want to do like the Norwegians do too?
    However, I recall a while ago someone said here in this site that maybe they are paid agents hired by this blog for pure entertainment in order to increase the number of visitors? That hypothesis hasn’t been falsified yet, hence maybe… who knows?
    🙂

  224. 224
    gpuccio says:

    Alicia:

    Hi! Long time, no see. I think I missed you, after all. In small doses, you know how to add fun to a discussion. 🙂

    (Too much of you. however…)

    OK, as I am still fresh with you at the moment, here are a few answers to your “comment”.

    My statement at #198:

    “Well, I have chosen myoglobin exactly because I think that it is a protein whose structure and function remain rather stable in vertebrates. Of course, some functional tweaking from species to species probably happens, but I think we can assume that the molecule needs no major engineering from species to species, and is passed on mainly passively. IOWs, it is probably not the object of new design in these transitions (of course, the molecule itself was designed in the beginning).”

    So, I am not saying that myoglobin is not designed. I am just saying that it was designed before the events I was considering.

    Now, you may believe that the functional information in myoglobin came by neo darwinian events. OK, I believe it came by design. But that is not the point here.

    The point is that, however that functional information arose, it is already there when the split between Synapsida and Sauropsida happens, about 300 million years ago. Indeed, human myoglobin shares 71% identities and 85% similarities with gekko, and with many other reptiles.

    So, the bulk of the information was already there. My point is simply that the variation from that point on is probably mostly neutral, even allowing for some functional tweaking. I think that is a point most biologists would agree on.

    So, I can see no reasons for your disagreement here. I have simply used neutral variation, and in particular ks values, to argue for common descent. Do you disagree?

  225. 225
    mw says:

    Further comments by Dr Ann Gauger:
    http://www.evolutionnews.org/2.....02927.html

  226. 226
    gpuccio says:

    Dionisio:

    Izumo 1 is a 350 AAs long protein (in humans), implied in sperm egg fusion.

    The human protein has rather strong sequence conservation in (non primate) mammals, ranging from 344 bits in mouse to about 500 bits in whales and dolphins, up to 541 bits in tupaia.

    In non vertebrates, the highest score is 154 bits in turtles, 134 bits in snakes, about 30 – 90 bits in fish.

    So, it seems that the protein underwent some radical transformation and informational jump at the level of mammals, therefore rather recently.

    The ka/ks analysis between human and mouse protein gives:

    ka = 0.4031348 ks = 1.088541 ka/ks = 0.3703442

    If you compare the ka/ks with the value for myoglobin (0.14346), you can see that izumo is much less conserved, even in mammals. It is a protein which changes much.

    Given the nature of the protein, and its probable species specificity, here it is not so easy to think that the differences are mainly neutral: functional species-specificity is very likely to play a big role.

  227. 227
    Dionisio says:

    gpuccio @224

    So, I am not saying that myoglobin is not designed. I am just saying that it was designed before the events I was considering.

    That was obviously understandable even to me!

    I’m a little surprised someone didn’t notice that? 🙂

  228. 228
    Dionisio says:

    gpuccio @224

    So, I can see no reasons for your disagreement here.

    Well, I do see a possible reason for your interlocutor’s pretended disagreement: an incomplete statement intentionally quoted out of context. Politicians do that too. 🙂

  229. 229
    Dionisio says:

    gpuccio @226

    Excellent explanation! Mile grazie!

  230. 230
    Alicia Cartelli says:

    So evolution can produce “some functional tweaking,” but this doesn’t qualify as “design,” however “we can assume that the molecule needs no major engineering,” but of course it was “designed in the beginning.”
    It can’t possibly be that millions of years of “some functional tweaking” produced a molecule that binds oxygen atoms, right?

    Take Izumo: mammals branched about 200mya, vertebrates about 500mya. That’s 300 MILLION years of molecular data from the vertebrates branching to the mammalian branch, which you are ignoring in comment 226.
    When you do some phylogenetic analyses that don’t involve skipping massive stretches of natural history, you let me know.

  231. 231
    Mung says:

    What makes evolution truly compelling is the lack of evidence for it. 300 MILLION years of missing evidence.

  232. 232
    gpuccio says:

    Alicia:

    “So evolution can produce “some functional tweaking,” but this doesn’t qualify as “design,” however “we can assume that the molecule needs no major engineering,” but of course it was “designed in the beginning.”
    It can’t possibly be that millions of years of “some functional tweaking” produced a molecule that binds oxygen atoms, right?”

    Right. It can’t possibly be. The increase in complexity from “some functional tweaking” to a complex functional sequence is exponential. Please, review your combinatorial calculus.

    “Take Izumo: mammals branched about 200mya, vertebrates about 500mya. That’s 300 MILLION years of molecular data from the vertebrates branching to the mammalian branch, which you are ignoring in comment 226.”

    I am ignoring nothing. I have simply stated the truth, that in mammals there is the appearance of at least 150 bits of new functional information. You can believe that it came through neo darwinian processes. I don’t (see above).

    “When you do some phylogenetic analyses that don’t involve skipping massive stretches of natural history, you let me know.”

    I am letting you know. I am skipping nothing.

  233. 233
    gilthill says:

    gpuccio

    As I was reading chapter 5 of “Darwin’s Doubt” by Stephen Meyer, I’ve learned that histones exhibit very little variation from one species to the next compared to other genes and therefore they are never used as molecular clocks. A possible explanation for this extreme conservation of histones would be to posit that these proteins are so essential to life that a very strong negative selection would apply to most non synonymous changes. But what about synonymous changes? A priori, there is no reason why the rate of synonymous changes should be lower for histones compared to other proteins such as myoglobin.
    But what is the real situation? What are the values of ka and ks for histones in the following cases: Pythos vs human; Gekko vs human; Gekko vs pythos; Mouse vs human?

  234. 234
    Alicia Cartelli says:

    “The increase in complexity from ‘some functional tweaking’ to a complex functional sequence is exponential.”
    This is where your lack of understanding in biology becomes a problem. First of all, get rid of the word “complex,” there’s no need for it. Second, how do you define a “functional sequence?” You realize that there is not a SINGLE functional sequence for any protein and definitely not for any function, right? Even highly conserved proteins have variation while retaining function and many systems within the cell are redundant; different proteins that have evolved separately, but carry out the same function. Evolution is too complex to just slap “combinatorial calculus” on it and say that’s how it works.

    “I am skipping nothing.”
    So saying that 150 bits arose “rather recently,” but ignoring the fact that theres about 300 million years between vertebrates branching and mammals branching doesn’t seem misleading to you? It’s either just another example of your extremely poor “science,” or of your complete lack of understanding. You had a better case with Prickle, but even then you were still skipping millions of years of evolution.

    I’ll put it this way: let me know when your jump in bits doesn’t coincide with a huge gap in sequence data.

    And just FYI gilthill, histones are not even close to “essential to life.”

  235. 235
    Dr JDD says:

    My car has 5 gears. 4 of them are redundant.

  236. 236
    Alicia Cartelli says:

    You just need one of them to get you where you want to go, so yeah, you’re right.

  237. 237
    Dr JDD says:

    Thank you for proving my point.

    Designers intentionally design redundancy for many reasons. One of them is the above example (efficiencies in different conditions).

  238. 238
    Eric Anderson says:

    Alicia @234:

    And just FYI gilthill, histones are not even close to “essential to life.”

    That is quite a claim, given their role in the cell.

    Do you think they are completely optional, nice to have, somewhat useful but unnecessary, highly useful but not critical? Or do they actually perform a key function that you imagine might not be “even close to essential”?

  239. 239
    Alicia Cartelli says:

    So because cells and cars both have redundancies, they are both designed JDD?
    In that case, chocolate and what my dog leaves outside every morning should taste the same because both are brown, right? Test that one out and get back to me.
    You conclude that these two things are similar based on them having a single thing in common. They are very different.

    EA, histones are nice to have, especially if you are looking to tightly regulate gene expression. They are not at all essential to life though, just ask one of the millions of bacterial species on this planet.

  240. 240
    Dr JDD says:

    No Alicia I did not say that. You were alluding in a previous post that redundancy is expected from evolution given we see a lot of redundant proteins in the cell. The inference was a designer wouldn’t do that.

    Yet you are so 1-dimensional in your thinking that you cannot seem to grasp the illustration that redundancy is not an argument against design. This is typical of naturalist.

  241. 241
    Alicia Cartelli says:

    What? When did I argue that redundancy is an argument against design?
    My argument is that redundancies in cells are an example of completely different proteins carrying out the same function. There is not “one single protein sequence” that carries out a specific function that evolution had to find, but in fact, there are many different sequences that can carry out any given function each with varying efficiency and specificity.
    I think you should sit this conversation out, you’re not even in the same ballpark.

  242. 242
    gpuccio says:

    gilthill:

    Here are the values for histone H3:

    Human – mouse:

    ka = 0.004670047 ks = 0.7436389 ka/ks = 0.006279992

    Human – gekko:

    ka = 0.009852407 ks = 0.8417407 ka/ks = 0.0117048

    Human – python:

    ka = 0.007994937 ks = 1.752374 ka/ks = 0.004562347

    Gekko – python:

    ka = 0.004842968 ks = 1.050345 ka/ks = 0.004610835

    As you can see, while ka values (and therefore ka/ks values) are extremely low, as expected given the extremely high conservation of the molecule, ks values are rather normal, like in any other protein. The only “unexpected” value is probably the human – gekko ks, which is definitely low (should be more like the human – python value), but of course we must expect some variance in individual cases. The general pattern of ks, however, is as expected even in histones.

  243. 243
    gpuccio says:

    Alicia:

    “First of all, get rid of the word “complex,” there’s no need for it.”

    Really? And what other words should I get rid of? Truth? Science? Reason?

    “Second, how do you define a “functional sequence?””

    Please, look here:

    http://www.uncommondescent.com.....n-defined/

    “You realize that there is not a SINGLE functional sequence for any protein and definitely not for any function, right? Even highly conserved proteins have variation while retaining function and many systems within the cell are redundant; different proteins that have evolved separately, but carry out the same function.”

    Yes I realize that, as do all those who are seriously in the ID field. Again, see here:

    http://www.uncommondescent.com.....n-defined/

    especially where it says:

    “e) The ratio Target space/Search space expresses the probability of getting an object from the search space by one random search attempt, in a system where each object has the same probability of being found by a random search (that is, a system with an uniform probability of finding those objects).”

    It’s you who apparently do not realize what ID theory is about. Ah, but I forgot… You have probably succeeded in getting rid of the word “complex”!

    “Evolution is too complex to just slap “combinatorial calculus” on it and say that’s how it works.”

    Complex? Hadn’t you succeeded in getting rid of that useless word? 🙂

    Let’s say that neo darwinism is too wrong to survive the “slapping” of combinatorial calculus, or any serious calculus for that.

    “So saying that 150 bits arose “rather recently,” but ignoring the fact that theres about 300 million years between vertebrates branching and mammals branching doesn’t seem misleading to you? It’s either just another example of your extremely poor “science,” or of your complete lack of understanding. You had a better case with Prickle, but even then you were still skipping millions of years of evolution.”

    Well, what I said is:

    “The human protein has rather strong sequence conservation in (non primate) mammals, ranging from 344 bits in mouse to about 500 bits in whales and dolphins, up to 541 bits in tupaia.

    In non vertebrates, the highest score is 154 bits in turtles, 134 bits in snakes, about 30 – 90 bits in fish.

    So, it seems that the protein underwent some radical transformation and informational jump at the level of mammals, therefore rather recently.”

    What is wrong in that? If the highest bit score with non mammals is 154 bits, why is it wrong to say that there is a gap of at least 150 bits with mammals?

    Of course the prickle proteins was a better case of information jump. But I have not offered Izumo 1 as a specialy good case of information jump. I was only answering Dionisio’s request about the evolutionary behaviour of that molecule, and I have reported what I found.

    But, if you really need some good example of information jump in vertebrates, please look at STAT 3, with its 1000+ bit jump from non vertebrates (highest bit score with humans 323, with a wasp) to vertebrates (highest bit score with humans 1391 for cartilaginous fish, 1419 for bony fish). That’s some information jump! 🙂

    “I’ll put it this way: let me know when your jump in bits doesn’t coincide with a huge gap in sequence data.”

    The only thing I can say is that my jumps in bits usually coincide with a huge gap in your understanding.

  244. 244
    Alicia Cartelli says:

    I know you love to throw around the word “complex,” but there’s no need for it here. We are looking for “function.” Period.
    Might as well get rid of the word “science” too, because there is certainly none of that here.

    You can send me to all the UD links you want, the problem is that your target space is way too narrow.The fact that proteins with very little in the way of sequence homology can carry out the same function should tell you just how large target spaces actually are in biology.
    Evolution does not look for a single sequence, nor a single target space, it is constantly testing the search space for anything that provides any type of advantage, which it then refines. You have no idea how to think about biology and it shows.

    Before we dig into this bit-jump crap again please re-state as clearly and succinctly as possible exactly what you are claiming, while taking into account the fact that turtles, snakes, and fish are all vertebrates.

  245. 245
    Dionisio says:

    gpuccio @243

    Really? And what other words should I get rid of? Truth? Science? Reason?

    Perhaps these words too?
    “specified, information, seriousness, consciousness, think, design, mind, humility, respect, meaning, purpose, understanding, sense, comprehensive, coherence, absolute, details, reading, explanation, clarity, spatiotemporal,… etc.”

    Complex? Hadn’t you succeeded in getting rid of that useless word?

    Ouch! That was a “Gotcha!” moment! 🙂

    The only thing I can say is that my jumps in bits usually coincide with a huge gap in your understanding.

    Yep. 🙂

    BTW, maybe your interlocutor can shed some light on how to produce Delta(d1) and Delta(d2) for this:
    Development(d1) = Development(ca) + Delta(d1)
    Development(d2) = Development(ca) + Delta(d2)
    Where “ca” stands for common ancestor.
    and d1, d2 are two of the descendants, as we discussed for your example of gekko and python?

  246. 246
    gilthill says:

    Thanks a lot gpuccio for these very interesting data at #242

  247. 247
    Dionisio says:

    #245 addendum

    Additional information on the ‘delta dev’ topic:

    It was first posted @206 @207 @214:
    http://www.uncommondescent.com.....ent-610470

    Any help with this will be very appreciated.

    Basically, describe in details a coherent and comprehensive way to get the two deltas. Pick any case, not necessarily gpuccio’s gekko vs. python. It could be cats and dogs, it it makes sense.

    Thank you.

    PS. The most recent evo-devo literature has quite a bit on this, but most of it ends up begging the questions “where’s the beef?” or “show me the money!” 🙂
    I want to see a serious description. Again, it must be comprehensive, coherent, detailed, and that holds water under any interrogation.

  248. 248
    gpuccio says:

    Alicia:

    “Before we dig into this bit-jump crap again please re-state as clearly and succinctly as possible exactly what you are claiming, while taking into account the fact that turtles, snakes, and fish are all vertebrates.”

    I thought it was clear:

    “But, if you really need some good example of information jump in vertebrates, please look at STAT 3, with its 1000+ bit jump from non vertebrates (highest bit score with humans 323, with a wasp) to vertebrates (highest bit score with humans 1391 for cartilaginous fish, 1419 for bony fish). That’s some information jump! :)”

    Turtles and snakes and birds have higher maximum homology than fish. That’s why I quoted fish, which are the oldest vertebrates. What’s your problem?

    On functional complexity, I will wait for when I have more time. In the meantime, please read the OP I linked. It could be a start.

  249. 249
    Alicia Cartelli says:

    My problem was when you said this:
    “In non vertebrates, the highest score is 154 bits in turtles, 134 bits in snakes, about 30 – 90 bits in fish.”
    …those are all vertebrates. But no biggie.

    Anyways, once again, your “information jump” occurs over millions of years. You compare a wasp, cartilaginous fish, and bony fish all to humans; let’s take a look:
    The nephrazoan split occured ~560mya, with one branch leading to wasps and the rest of the protostomes, while the other continued on to fishes, humans and the rest of the deuterostomes.
    The split between humans and cartilaginous/bony fish occured 460-430 mya.
    This leaves us with approximately 100 million years to explain the 1000+ bit jump in wasps to the fishes.
    100 MILLION years…

    So, once again, let me know when your jump in bits doesn’t cover 100+ million years of natural history.

  250. 250
    gpuccio says:

    Alicia:

    Ah, I thought you were speaking of the stat 3… I had not realized the mistake in my post #226, where of course I meant “non-mammals”, and not “non-vertebrates”. Thank you for the correction.

    Regarding stat 3, the 323 bits hit with the wasp is the highest score when blasting the human protein against all metazoa, excluding vertebrates. For example, the highest score in tunicates is 270, while best in hemichordates is 302.

    Indeed, those “low” scores in non vertebrates are not with a true stat3 molecule, but rather with various isoforms of stat 5b, a protein which exists in humans too (the two human proteins share indeed 313 bits of homology).

    IOWs, stat3 does not exist in non vertebrates, and has a low homology of about 300 bits with stat 5b, which instead is already present in non vertebrates.

    So, your reasoning about wasps needs to be reviewed. We see no trace of stat 3, with its 1000+ new bits of functional information, before the appearance of vertebrates, not even in the closest precursors, tunicata or cephalochordata.

    However, that is not really the point. If you want 100 million years to explain the appearance of those 1000+ bits, I am ready to concede them to you. Why? Because not even with 100 billion years available you could explain that. Have you ever wondered why so many of your darwinist friends are putting their last few hopes in the multiverse?

    The point is, 1000 bits is well beyond any universal probability bound, even the most conservative.

    Abd do me a favor, just blast stat 3 human vs mouse, and have a look at what happened to the molecule in the last 70 – 80 million years, because it’s really amazing:

    Stat 3 human vs mouse: 769 identities out of 770 AAs. 770 similarities (100%).

    Amazing is an understatement: this is stuff which shames any histone!

    Now, before you go berserk with the redundancy idea, embarrassing yourself even more, just give a look at this recent OP:

    http://www.uncommondescent.com.....ot-simple/

    which, IMO, did not receive the attention it deserved, and read the linked paper. Just as a background, OK?

    Well, and now please answer the following simple question:

    If, as the paper suggests, the tryptophan synthase complex arose about 3.5 billion years ago, in less than 500 million years, and was already extremely similar to the present form in terms of function, then how can you explain that it went lost in all animal metazoa, while surviving in prokaryota, single celled eukaryota and plants?

    IOWs, if evolution is so clever in finding functional sequences, among the many redundant ones that in your opinion can perform the same function, and that, always in your opinion, make the target space so much bigger than I believe, then why in about 1 billion years no animals have developed some new form of tryptophan synthase?

    Hear me, we are not discussing something trivial: tryptophan is one of the 20 AAs which form all the proteins in all living beings. Metazoa cannot live without it, and so for them it becomes an essential aminoacid: IOWs, they have to take it from the environment. There is no doubt that being able to synthesize it would be a real advantage.

    But, for some strange reason, that single molecular complex which so easily came out of the primordial earth, traversing OOL and some hundred million years to come into existence, has not been found again in metazoa. Not even some poorer substitute, among the billions of billions of molecules able to perform the same function which live in Alicia Cartelli’s imagination.

    We are not even discussing some extremely complex molecule: just two chains, in E. coli 268 + 397 AAs, which make up a 4 chain structure. The alpha chain is not even much conserved up to plants, while the beta chain shows greater conservation (56% identity between E. coli and Arabidopsis). Piece of cake, for an evolution which can make stat3 in less than 100 million years!

    And yet, animalia still remain deprived of tryptophan synthase. Can you explain it?

    Redundancy, redundancy… Maybe just the expression of clever design to make robust implementation, rather than the forest of functional sequences that you seem to dream of?

    .

  251. 251
    bill cole says:

    gpuccio

    However, that is not really the point. If you want 100 million years to explain the appearance of those 1000+ bits, I am ready to concede them to you. Why? Because not even with 100 billion years available you could explain that. Have you ever wondered why so many of your darwinist friends are putting their last few hopes in the multiverse?

    How do you calculate the 1000 bits?

    If you have a 770 AA protein and 100 billion years and a population of 10^7 then how much of this space can evolution explore. My thought is 1/20^770 divided by 10^11 x10^7 or around 1/20^755 which is an imaginary number since it is a smaller ratio then an election divided by the size of the universe measured in elections. So how much of this space can evolution explore? For all intent and purposes, none of it.

  252. 252
    gpuccio says:

    bill:

    The 1000 bit value is derived from the difference in bitscore given by the blast software. As said, the highest bitscore with the human protein in non vertebrates is about 300, while the highest bitscore in cartilaginous fish, the oldest vertebrates, is 1391. That means more than 1000 bits of functionality difference between non vertebrates and vertebrates.

    Computing the bitscore of homology between two distant proteins is a very simple way to measure the functional constraints on that sequence, IOWs its functional complexity.

    The 1391 bitscore between shark and humans means a high functional complexity. In 400+ million years, any non functional sequence will become unrecognizable in two separate lines (for example, ks values usually reach saturation in that span of time). So, a conserved sequence is a very good measure of functional constraints.

    By the way, the Blast bitscore takes in consideration also the number of comparisons in the protein database.

    For all these reasons, the bitscore between two distant lineages is a very good measure of the functional complexity of the sequence, IOWs of the target space / search space ratio.

    In the case of stat 3, if we allow that 300 bits of its functional information were already present in the non vertebrate stat 5b molecule, more than 1000 bits of functional information remain to be explained in the vertebrates stat 3, as it appears in skarks.

    Of course, that is less than the total information in the molecule, which is about 3000 bits. 1000 bits is a measurement of functional information, not of total information.

    According to a gross and generous computation, the highest space that can be searched by evolution in the whole life span of our planet is, at best, 120 bits. And that is for prokaryotes. I suppose that your assumption of a searched space of about 60 bits for a meatazoan population in 100 million years is quite reasonable. That still leaves about 1000 bits of functional information to be explained, just in the stat 3 molecule. 🙂

  253. 253
    Dionisio says:

    gpuccio @252

    Clear explanation, as usual. Thank you.

    You closed your comment saying “…just in the stat 3 molecule.”
    Does that mean other protein molecules could be analyzed and lead to similar conclusions, though different value ranges?

    Are the parts that don’t match either nonfunctional or functional only for a particular kind of biological systems, but not for all?

    Is that analysis done on the actual proteins resulting from the post-translational modifications and folding?
    Is this because proteins are kind of like the workhorses of biology and also recognizable cellular biomarkers?

    Are there similar functional analyses done on ncRNA which deal mainly with regulatory processes as some proteins do?

    Are references to biological functions related to how things work or what results they produce or both?
    IOW, are the terms function and purpose interchangeable?

  254. 254
    Alicia Cartelli says:

    “So, your reasoning about wasps needs to be reviewed.”
    No, it doesn’t if you want to compare wasps and fishes to humans like this, then I am correct to trace their lineages back to where they branched off from what would give rise to humans, look at the date and compare them. Your “jump” in bits occurs over millions of years, just as it did with prickle.
    And here we go again with the “search space is too big to get this specific sequence” argument. I love when you guys make that argument because it demonstrates how clueless you guys actually are. Evolution was not looking for that specific sequence and it does not need that specific sequence, not even close. The majority of amino acids in any protein can be swapped out and function will be retained. You guys underestimate functional sequence space so badly that it’s laughable.
    Wow, 99.9% similarity in mice and humans….so a protein that evolved into an important functional niche has remained there and retained it’s sequence…shocking….

    “And yet, animalia still remain deprived of tryptophan synthase. Can you explain it?”
    The lineage giving rise to Animalia lost it and other adaptations have taken over the role of providing tryptophan. Adaptations that allow them to take in food, to move, to digest food, all of these things made tryptophan synthase expendable and therefore also lowered the selective pressure on organisms to re-evolve the complex.
    You guys are too simple minded when it comes to the complexities of life and its evolution, sorry.

  255. 255
    gpuccio says:

    Alicia:

    ““So, your reasoning about wasps needs to be reviewed.”
    No, it doesn’t if you want to compare wasps and fishes to humans like this, then I am correct to trace their lineages back to where they branched off from what would give rise to humans, look at the date and compare them. Your “jump” in bits occurs over millions of years, just as it did with prickle.”

    Well, of course a jump occurs over millions of years, for the very simple reason that we cannot get any precise resolution of times in natural history, at those time distances. That’s why I conceded some 100 million years. What I meant is that the split between humans and fish is not the same thing as the split between humans and wasps.

    Now it becomes really funny. 🙂

    How can you just make the following two statements, one after the other?

    1) “The majority of amino acids in any protein can be swapped out and function will be retained. You guys underestimate functional sequence space so badly that it’s laughable.”

    and:

    2) “Wow, 99.9% similarity in mice and humans….so a protein that evolved into an important functional niche has remained there and retained it’s sequence…shocking….”

    (emphasis mine).

    Well, what is really shocking is your logic. Now, please, tell me:

    How is it that a protein has remained the same for 70 million years, exactly the same, 769 AAs out of 770 (OK, one changed to a similar AA!), if “the majority of amino acids in any protein can be swapped out and function will be retained”?

    I can’t follow you.

    Excuse me, the sequence in the stat 3 gene in those 70 million years was subject to neutral changes just like any other sequence, wasn’t it? So, many AAs in it should have been swapped out in that span of time, and function should have been retained.

    So, why didn’t that happen?

    If you understand the basics of evolutionary thinking, you should admit that there is only one possible reason: each single non synonimous change which occurred by chance in the sequence in those 70 million years did not survive or be fixed by drift for the very simple reason that it was not neutral, and not even nearly-neutral: those changes, which certainly took place, were consistently eliminated by negative purifying selection, because they were deleterious and function was seriously affected.

    Do you know what is the value of the ka/ks for human stat 3 vs mouse?

    It is 0.001545962. That means that non synonimous mutations, in those 70 million years, were almost 1/1000 if compared with synonimous mutations. (ka is 0.000671891, while ks is 0.4346101).

    That means that negative selection was really active on this molecule, in those 70 million years. How can you explain that simple observable fact?

    Shocking, isn’t it?

    “The lineage giving rise to Animalia lost it and other adaptations have taken over the role of providing tryptophan. Adaptations that allow them to take in food, to move, to digest food, all of these things made tryptophan synthase expendable and therefore also lowered the selective pressure on organisms to re-evolve the complex.”

    Ah, that is scientific reasoning at its best! Tryptophan synthase expendable!

    I will not even comment on that, out of simple compassion.

  256. 256
    gpuccio says:

    Dionisio:

    “Does that mean other protein molecules could be analyzed and lead to similar conclusions, though different value ranges?”

    Of course! A lot of them. The appearance of new complex information is not limited to the appearance of new genes. It takes place, mostly, through changes to existing genes, appearance of new sequences in them, or radical transformations of the existing sequences for functional reasons. That is especially true for regulatory proteins.

    “Are the parts that don’t match either nonfunctional or functional only for a particular kind of biological systems, but not for all?”

    Part of the variation we observe is neutral variation, according to standard neutral theory. But a great part of the variation is functional. If some important variation becomes conserved for millions of years in some lines, it is certainly functional. That’s a way to distinguish between neutral variation and functional variation.

    And yes, functional variation is often conserved in a taxonomically restricted way. I have shown that for prickle protein (see here):

    http://www.uncommondescent.com.....ted-genes/

    And I am gathering new examples, which I will probably include in some new OP.

    “Is that analysis done on the actual proteins resulting from the post-translational modifications and folding?
    Is this because proteins are kind of like the workhorses of biology and also recognizable cellular biomarkers?”

    All my analyses are done on the Reference Sequences for the protein and for its mRNA (coding part), usually from the NCBI RefSeq database.

    “Are there similar functional analyses done on ncRNA which deal mainly with regulatory processes as some proteins do?”

    Working on ncRNA is more difficult. Ka and ks cannot apply there. It’s much more difficult to compare sequences too, because here is much more variability. And much less is known about the functions. For the moment, I am sticking to protein coding genes for my personal molecular reasonings.

    Of course, there is a lot of literature about ncRNAs. I am trying to look at it in detail, from an ID point of view. I am confident that all important molecular findings in biology are strong evidence for ID. We just need to look at them with attention, and with the right perspective.

    “Are references to biological functions related to how things work or what results they produce or both?
    IOW, are the terms function and purpose interchangeable?”

    Good question!

    As I see it, purpose and function are two related concepts, but there is a definite difference:

    a) Purpose is a subjective experience, a form of conscious experience, and in particular a form of feeling connected to some special cognitive content: very simply, it is the desire to get some specific meaning objectively implemented.

    All of that happens in the designer’s consiousness.

    b) Function is the objective implementation of some specific configuration in some material object that makes it possible to obtain the above mentioned desired result through that object.

    That happens in the objective world, without any need of any subjective intervention, once the designed configuration has already been implemented into the material object.

    IOWs, tryptophan synthase goes on synthesizing tryptophan in the objective world, after its designed appearance in biological beings.

    So, there is no need of any conscious being for the designed object to work, and to get its specific result. The designe object is a machine.

    But we need some conscious observer to recognize the function in the machine, to understand that it is a specific configuration which gets a specific result, and to hypothesize that such a result is a desired result which was implemented by some conscious being through the designed object/machine.

    Of course, the functional complexity approach allows us to make a safe design inference, and to give objective support to our hypothesis.

  257. 257
    bill cole says:

    Alicia

    And here we go again with the “search space is too big to get this specific sequence” argument. I love when you guys make that argument because it demonstrates how clueless you guys actually are. Evolution was not looking for that specific sequence and it does not need that specific sequence, not even close. The majority of amino acids in any protein can be swapped out and function will be retained. You guys underestimate functional sequence space so badly that it’s laughable.

    If this is true then why are single mutations often fatal in nuclear proteins. These proteins interact in order to control functions like cell division. If the sequence is off they cannot fit together with charge and shape to perform their proper function. The unique sequences allows these proteins to work together. If you read page 50 of the blind watchmaker you will see that Richard Dawkins acknowledges this issue and tries to solve it with his Weasel program. Evolutionary biologist Art Hunt also wrote a paper that supports the rarity of protein folds in sequential space.

  258. 258
    Alicia Cartelli says:

    Pucci, how many times do I have to tell you, there is a difference between maintaining “function” and maintaining “optimal function.”
    Things does not evolve at the same rate either (species or molecules). There can be periods of both relatively fast evolution and relatively slow, depending on the selective pressures faced, what the molecule does, and many other things. Function does not have to be “seriously affected” for purifying selection to take place over those timescales. In important mechanisms such as the development and the immune system (STAT3) evolution will find the optimal structure and function, and then retain it. You consistenlty make the same mistakes and the same incorrect assumptions.

    “Tryptophan synthase expendable! I will not even comment on that, out of simple compassion.”
    I hope it’s expendable (under the right conditions), because you and I sure as hell don’t have it.
    If you have an issue with my explanation, feel free to state it.
    Please keep things short and sweet, I won’t be here much longer.

    Bill, most proteins consist of hundreds of amino acids, many of these amino acids can be swapped out for other amino acids and the protein will still function. Proteins have been re-built in the lab using only three different amino acids I think it was. There is a small subset of amino acids in each protein that are absolutely essential for function, and even some of these can be swapped out with others while retaining function as long as you swap it out with an amino acid of the same type. Often mutations in these amino acids do not result in a similar amino acid being switched in, and this can drastically reduce function or frameshift mutations can occur in which the entire sequence is thrown off. There are many different cases, each with different effects. Learn more about proteins if you want to understand this, enzymes have active sites, interacting proteins have binding sites, these are where you’ll find the amino acids that are more specific for function whereas the rest of the protein (the majority of it) can often be varied with little to no change in function.

  259. 259
    bill cole says:

    Alicia

    Bill, most proteins consist of hundreds of amino acids, many of these amino acids can be swapped out for other amino acids and the protein will still function. Proteins have been re-built using only three different amino acids I think it was. There is a small subset of amino acids in each protein that are absolutely essential for function, and even some of these can be swapped out with others while retaining function as long as you swap it out with an amino acid of the same type. Often mutations in these amino acids do not result in a similar amino acid being switched in, and this can drastically reduce function or frameshift mutations can occur in which the entire sequence is thrown off. There are many different cases, each with different effects. Learn more about proteins if you want to understand this, enzymes have active sites, interacting proteins have binding sites, these are where you’ll find the amino acids that are more specific for function whereas the rest of the protein (the majority of it) can often be varied with little to no change in function.

    This claim is extraordinary. Most proteins need to bind to other proteins or small molecules. The nuclear pore complex will not allow proteins to pass with single mutations per experiments at UC Berkeley. The minimum probability of a protein just being able to bind ATP for an 80 amino acid protein is 1/10^12 per Jack Szostak’s origin of life research. You have created a story here and if you have evidence that makes your claim more then a “just so” story I would be interested. If not you need to wake up and smell the coffee that current evolutionary theory is almost certainly wrong.

  260. 260
    mike1962 says:

    “Alicia”: Pucci, how many times do I have to tell you, there is a difference between maintaining “function” and maintaining “optimal function.”

    Notice how “Alicia” bounced right past Gpuccio’s very precise question:

    How is it that a protein has remained the same for 70 million years, exactly the same, 769 AAs out of 770 (OK, one changed to a similar AA!), if “the majority of amino acids in any protein can be swapped out and function will be retained”?

    So, “Alicia”, are you making the claim that the 769 unchanged AAs were required unchanged
    for mere function – as opposed to optimized function – over that span of time?

  261. 261
    Origenes says:

    Cartelli: There is a small subset of amino acids in each protein that are absolutely essential for function, and even some of these can be swapped out with others while retaining function as long as you swap it out with an amino acid of the same type.

    Repeating the same refuted mantra is pathetic and does not constitute a response. It is as if Cartelli is completely unable to absorb the facts:

    GPuccio:

    How is it that a protein has remained the same for 70 million years, exactly the same, 769 AAs out of 770 (OK, one changed to a similar AA!), if “the majority of amino acids in any protein can be swapped out and function will be retained”?

    – – –
    edit: Mike1962 @260, indeed! 🙂

  262. 262
    Alicia Cartelli says:

    So, Bill, the NPC binds a specific sequence in nuclear proteins, this would be the small subset of amino acids that are essential for that protein’s function, which is exactly what I said 10 minutes ago. And Szostack concluded that ATP-binding proteins could be found by randomly sampling protein space. I have not created a story, I’m trying to teach you basic biology.

    Mike, as I said, the retention of those 769 amino acids is due to the fact that the protein’s OPTIMAL function is highly important for the organism, that does not necessarily mean that those amino acids are essential to have any function (there’s a difference). STAT3 is involved in development and the immune system. A less-than-optimal STAT3 is still functional, but over the course of evolution (millions of years), even only a slightly less optimal protein will be bounced out of the population eventually, due to the protein’s roles in an organism. You guys really do need to be spoonfed.

  263. 263
    bill cole says:

    Alicia

    So, Bill, the NPC binds a specific sequence in nuclear proteins, this would be the small subset of amino acids that are essential for that protein’s function, which is exactly what I said 10 minutes ago. And Szostack concluded that ATP-binding proteins could be found by randomly sampling protein space. I have not created a story, I’m trying to teach you basic biology.

    The NPC is a gate it does not bind proteins. How do you know what code the NPC is using to open or shut? Have you studied experiments here? Yes, Szostak said they could be found with a probability of 1/10^12 for 80 amino acids. IMHO a very low probability for one necessary but not sufficient protein function. What area of biology is your expertise?

  264. 264
    Alicia Cartelli says:

    “The NPC is a gate it does not bind proteins.”
    Are you kidding me, Bill? Please stop before you embarrass yourself any further. Proteins binding each other is everything, whether it’s the NPC or hemoglobin.
    Google these and then get back to me:
    Nuclear export signal
    Nuclear import signal
    nucleoplasmin
    That should be a good start

    “IMHO a very low probability”
    Obviously no one should care what your “humble opinion” is when it comes to biology.

  265. 265
    mike1962 says:

    “Alicia:” Mike, as I said, the retention of those 769 amino acids is due to the fact that the protein’s OPTIMAL function is highly important for the organism, that does not necessarily mean that those amino acids are essential to have any function (there’s a difference). STAT3 is involved in development and the immune system. A less-than-optimal STAT3 is still functional, but over the course of evolution (millions of years), even only a slightly less optimal protein will be bounced out of the population eventually, due to the protein’s roles in an organism.

    So then, what you seem to be saying is that your statement, “The majority of amino acids in any protein can be swapped out and function will be retained”, should be changed to, “The majority of amino acids in any protein can be swapped out and function will be retained… but any swapped out AAs will not accumulate or persist when optimal function is ‘highly important.’” Right?

  266. 266
    Alicia Cartelli says:

    Sure Mike.

  267. 267
    gpuccio says:

    Alicia:

    I think you are now completely out of your mind.

    Simple comments:

    “Things does not evolve at the same rate either (species or molecules). ”

    But neutral evolution goes on anyway. Again, how is it that we have such a low ka/ks for stat 3? You have not answered.

    “Function does not have to be “seriously affected” for purifying selection to take place over those timescales.”

    You must be kidding. Purifying selection happens only if there is a real reproductive disadvantage. That is certainly a serious reduction in function.

    “Proteins have been re-built in the lab using only three different amino acids I think it was.”

    ??? Exact reference, please. Otherwise, you are out of any discussion with me.

    “I hope it’s expendable (under the right conditions), because you and I sure as hell don’t have it.”

    What a reasoning! Then human intelligence is expendable (animals exists without it). Flight is expendable (we don’t fly). A lot of metabolic pathways, practically all those which are not universal, are expendable. And why would tryptophan synthesis be expendable, and not all other aminoacid pathways? After all, we can get other aminoacids from our food, just like tryptophan.

    And so on, and so on. I have never seen a case of such blatant ad hoc reasoning as yours.

    And your distinction between “function” and “optimal function” is really pitiful. What do you mean, that vertebrate stat 3 evolved in your (conceded) 100 million years through hundreds of states of partial function, which obviously were perfectly compatible with life, but exist today only in your mind, and for some reason in cartilaginous fish it had achieved “optimal function”, so that any even partial regress to previous functional states was incompatible with survival?

    I don’t know what you are: either a fool, a mythomaniac, or simply a confused dogmatist. Whatever, this is really too much.

    Please, give that reference, or we are done.

  268. 268
    mike1962 says:

    Gpuccio to “Alicia”: And your distinction between “function” and “optimal function” is really pitiful. What do you mean, that vertebrate stat 3 evolved in your (conceded) 100 million years through hundreds of states of partial function, which obviously were perfectly compatible with life, but exist today only in your mind, and for some reason in cartilaginous fish it had achieved “optimal function”, so that any even partial regress to previous functional states was incompatible with survival?

    This was essentially my next reply to “Alicia.” I’d like to see a definition of what ‘highly important’ means that isn’t ad hoc or tautological. Without evidence, it is merely an ad hoc excuse, not an explanation, for why some AAs are conserved over vast amounts of time and some are not, esp given that life is full of situations where functionality and more optimized functionality co-exist just fine even when they are competing for the same resources. For “Alicia” it must boil down to something like, “well it must have happened this way because how else could it have happened?”

    Keep up the good work, gpuccio.

  269. 269
    Dionisio says:

    gpuccio @256
    Thank you for the insightful explanation.

    Do some functions seem sufficiently robust in order to operate within highly stochastic biological scenarios under strong thermodynamic/biochemical noise, in order to produce the results that correspond to some apparent purpose?

    Has that been observed in any of the latest discoveries made by the researchers of developmental processes in biological systems lately?

    BTW, once the ongoing discussion on the appearance and conservation of complex specified functional information associated with DNA, mRNA, proteins, etc. gets settled for good, can we look carefully at the evo-devo developmental issue we briefly mentioned before in this thread:

    Knowing Dev(ca), how to setup Delta(d1) and Delta(d2) in order to get Dev(d1) and Dev(d2)
    Dev(d1) = Dev(ca) + Delta(d1)
    Dev(d2) = Dev(ca) + Delta(d2)
    Where “ca” is a common ancestor for descendants d1 and d2?

    Obviously, that must require a most comprehensive knowledge of Dev(ca), Dev(d1) and Dev(d2). Are we there yet? 🙂

    The current evo-devo literature has quite a bit of that stuff, but it’s mostly like in Mina’s famous song “parole, parole, parole!” 🙂

    I want to see something more concrete that can be simulated on computers and/or animated for educational purposes.

    Now that the 100 petaflops barrier for supercomputers has been broken, more Big Data processing for biological simulations should be possible.
    It’s getting really exciting in biology research.

  270. 270
    Dionisio says:

    gpuccio

    RE: http://www.uncommondescent.com.....low-dance/

    Does that mean the given proteins were available and conserved long before they were needed?

    This reminds me a time when we released programs that contained features for future releases, but the users didn’t know they were in there already. 🙂

  271. 271
    bill cole says:

    Alicia
    I am not sure why we are mis communicating it may be my issue. The main function of the nuclear pore complex is to manage the import and export of molecules inside and out side the nucleus or act as a gate to protect the nucleus. It also appears to manage flow rates in and out of the nucleus.

    Small particles ~40 kDa) are able to pass through the nuclear pore complex by passive diffusion. Larger particles are also able to pass through the large diameter of the pore but at almost negligible rates.[14][15] Efficient passage through the complex requires several protein factors.[16] Karyopherins, which may act as importins or exportins are part of the Importin-? super-family which all share a similar three-dimensional structure.

    Three models have been suggested to explain the translocation mechanism:

    Affinity gradients along the central plug
    Brownian affinity gating
    Selective phase

    Here is an explanation of the sequences that allow protein import

    Classical NLSs can be further classified as either monopartite or bipartite. The first NLS to be discovered was the sequence PKKKRKV in the SV40 Large T-antigen (a monopartite NLS).[1] The NLS of nucleoplasmin, KR[PAATKKAGQA]KKKK, is the prototype of the ubiquitous bipartite signal: two clusters of basic amino acids, separated by a spacer of about 10 amino acids.[2] Both signals are recognized by importin ?. Importin ? contains a bipartite NLS itself, which is specifically recognized by importin ?. The latter can be considered the actual import mediator.

    Chelsky et al. proposed the consensus sequence K-K/R-X-K/R for monopartite NLSs.[2] A Chelsky sequence may, therefore, be part of the downstream basic cluster of a bipartite NLS. Makkerh et al. carried out comparative mutagenesis on the nuclear localization signals of SV40 T-Antigen (monopartite), C-myc (monopartite), and nucleoplasmin (bipartite), and showed amino acid features common to all three. The role of neutral and acidic amino acids was shown for the first time in contributing to the efficiency of the NLS.[3]

    Rotello et al. compared the nuclear localization efficiencies of eGFP fused NLSs of SV40 Large T-Antigen, Nucleoplasmin (AVKRPAATKKAGQAKKKKLD), EGL-13 (MSRRRKANPTKLSENAKKLAKEVEN), c-Myc (PAAKRVKLD) and TUS-protein (KLKIKRPVK) through rapid intracellular protein delivery. They found significantly higher nuclear localization efficiency of c-Myc NLS compared to that of SV40 NLS.[4]

    Alicia, how would you explain the evolution of this mechanism through modern evolutionary theory? One wrong mutation and the protein cannot import or the RNA cannot export.
    The signal is 4^46 of organized nucleic acids per protein. What mechanism do you propose that created this sequence so it would be recognized by the NPC which is 4^150k of possible nucleotides that need to be organized to create this transport mechanism.

    Just to bind ATP the probability is 1/10^12 per 80 amino acids. You are looking at a protein complex of greater then 50K amino acids that binds at multiple sites. I don’t believe that RMNS or neutral mutations could build this, do you?

  272. 272
    MatSpirit says:

    Has anybody read PaV’s June 19th “The War is Over: We Won!” post?

    Apparently, if we lose genes, evolution has lost the war!

    Personally, I have faith in PaV’s ability to get things wrong.

  273. 273
    Querius says:

    MatSpirit sure sounds a lot like rvb8. And Alicia’s assertion is priceless!

    Things does not evolve at the same rate either (species or molecules).

    Oh, I get it. This is the survival of the fittest molecule, which can then reproduce itself as a result.

    Dr. Strangelove does Darwin comes next. O.o

    -Q

  274. 274
    MatSpirit says:

    Nope, not me. I do recommend you read the “War is Over” thread though if you’re interested in lost genes.

  275. 275
    Alicia Cartelli says:

    “But neutral evolution goes on anyway. Again, how is it that we have such a low ka/ks for stat 3? You have not answered.”
    Yes, I did, you must not like to read.
    I said that STAT3 has maintained it’s sequence because of its importance in both development and the immune response. Small changes in the sequence of this protein do not mean a loss of function, but they can lower function enough so as to alter the development or the immune reponse. Negatively effecting these processes does not mean immediate selcection against, but over the timescales of millions of years, the changes will be selected against. This is what preserves these protein’s sequences.

    “Exact reference, please”
    I mention this research pretty much every time I come to UD. Obviously you are impermeable to knowledge.
    The David Baker lab did the work I was referring to, but it was 5 amino acids. They found that for some proteins, substitutions were tolerated at 95% of amino acids.

    Yes, these things are all expendable, as I said, depending on conditions. Certain amino acids are essential for us and certain ones are not because of our evolutionary past. Certain amino acids were abundant for our ancestors and the pathways to make those molecules became expendable. The loss of those pathways remains in the ancestors of those species, which includes us.

    “And your distinction between “function” and “optimal function” is really pitiful.”
    They are two very different things, the first is simply the protein’s ability to carry out it’s molecular function, such as bind DNA or another protein, or both, whatever. The second takes into account the protein’s role in a certain pathway and the effect on the species if teh protein undergoes changes. These two things do not always change in a 1:1 ratio. You simpy don’t have a good enough grasp on molecular biology, nor an evolutionary perspective wahtsoever.

    Bill, for the last time, the NPC importing things and exporting things is controlled by protein interactions via localization signals. That’s proteins BINDING to each other and the sequences can be very different, as you can see by the localization signals in your own quote.

    “I don’t believe”
    Like I said, when it comes to biology, nobody cares what you “believe in.”

  276. 276
    gpuccio says:

    Alicia:

    The reference, please. Exact reference to the paper. Otherwise, I will not go on discussing with you.

  277. 277
    Alicia Cartelli says:

    http://www.nature.com/nsmb/jou.....7-805.html
    Took me all of five seconds to find it pucci.

  278. 278
    Eric Anderson says:

    Oooh, another literature bluff! How fun!

  279. 279
    bill cole says:

    Alicia

    arly protein synthesis is thought to have involved a reduced amino acid alphabet. What is the minimum number of amino acids that would have been needed to encode complex protein folds similar to those found in nature today? Here we show that a small beta-sheet protein, the SH3 domain, can be largely encoded by a five letter amino acid alphabet but not by a three letter alphabet. Furthermore, despite the dramatic changes in sequence, the folding rates of the reduced alphabet proteins are very close to that of the naturally occurring SH3 domain. This finding suggests that despite the vast size of the search space, the rapid folding of biological sequences to their native states is not the result of extensive evolutionary optimization. Instead, the results support the idea that the interactions which stabilize the native state induce a funnel shape to the free energy landscape sufficient to guide the folding polypeptide chain to the proper structure.

    How do you think this paper supports your position that RMNS is the cause of diversity?

  280. 280
    Dr JDD says:

    Alicia @ 277:

    What exactly are you claiming that reference demonstrates? That the sequence space for a specified functional protein is vast (only 5 aa necessary)?

    It seems to me that you are stretching what the Baker paper you referenced demonstrates. It seems to only show that 5aa are necessary to get the simple beta-barrel fold found in an SH3 domain. It also shows that some of the substituted forms based on a simple aa availability can fold as fast or even faster than wt and show good stability. The problem is, a beta-barrel is not a function. It is a structural feature or a type of protein fold. Has anyone put this into a functional protein with a beta-barrel and demonstrated function is retained (at a rate reasonable for a cellular function)?

    Interestingly, the authors state in the introduction when referring to alpha helices:

    “In complementary studies, entire helical bundle architectures have been built from reduced amino acid alphabet but for the most part they do not appear to have the ordered packing characteristic of biological proteins.”

    Note the last part of the sentence.

  281. 281
    Dr JDD says:

    Let me clarify my question in post 280 (as I know where you will take this if I do not clarify):

    I am referring to the function of the entire protein and also physiologically relevant function.

    I am aware they isolated mutants through binding to proline rich peptides immobilised on beads but this is neither physiological nor difficult to achieve or very meaningful. Certainly though, it is not something that demonstrates 95% of a protein can be mutated and still retain its function. That is a very misleading and false assessment.

  282. 282
    Alicia Cartelli says:

    That is the “exact reference to the paper” that pucci asked for.
    Don’t all get your panties in a bunch now.

  283. 283
    gpuccio says:

    Alicia:

    Your initial statement:

    “Bill, most proteins consist of hundreds of amino acids, many of these amino acids can be swapped out for other amino acids and the protein will still function. Proteins have been re-built in the lab using only three different amino acids I think it was.”

    The paper you link (the abstract, the rest is paywalled):

    “Functional rapidly folding proteins from simplified amino acid sequences

    David S. Riddle1, Jed V. Santiago1, Susan T. Bray-Hall1, Nikunj Doshi1, Viara P. Grantcharova1, Qian Yi1 & David Baker1, ,2

    Abstract
    Early protein synthesis is thought to have involved a reduced amino acid alphabet. What is the minimum number of amino acids that would have been needed to encode complex protein folds similar to those found in nature today? Here we show that a small beta-sheet protein, the SH3 domain, can be largely encoded by a five letter amino acid alphabet but not by a three letter alphabet. Furthermore, despite the dramatic changes in sequence, the folding rates of the reduced alphabet proteins are very close to that of the naturally occurring SH3 domain. This finding suggests that despite the vast size of the search space, the rapid folding of biological sequences to their native states is not the result of extensive evolutionary optimization. Instead, the results support the idea that the interactions which stabilize the native state induce a funnel shape to the free energy landscape sufficient to guide the folding polypeptide chain to the proper structure.”

    You are really a buffoon. Dr JDD has already commented very well. If I had access to the details of the paper, I would comment more in detail.

    If it were true that proteins can be rebuilt with 5 aminoacids, and remain functional, why don’t they do it? It should be so easy to build libraries of functional proteins with 5 AAs only.

    You are not capable of any serious and respectful discussion, and your only partial excuse could be that your understanding of biology is really ridiculous.

  284. 284
    Alicia Cartelli says:

    “If it were true that proteins can be rebuilt with 5 amino acids….”
    Pucci, it is true. I just sent you the paper, which you demanded, that showed exactly that. Do you live in a constant state of denial of scientific evidence or do you just have the attention span of a goldfish?
    And now you move the goalposts, demanding “libraries” of functional proteins. You obviously have no idea how experimental biology works.
    It’s not me with a lack of understanding in biology, it’s you. Sorry to burst your bubble.

  285. 285
    bill cole says:

    Alicia

    “If it were true that proteins can be rebuilt with 5 amino acids….”
    Pucci, it is true. I just sent you the paper, which you demanded, that showed exactly that

    Do you really believe that the paper submitted supports this? You made a claim that we could create protein structures with 3 amino acids yet your paper refutes your claim. Whats going on? When you say proteins do you mean that all 100000 human proteins only require 5 amino acids? The paper you cited is 19 years old. Do you have any follow up supporting evidence?

  286. 286
    Alicia Cartelli says:

    Billy, are you kidding, I said I wasn’t sure if it was three originally. So it’s five. Either way it’s a fraction of what is used by living organisms today. Are you so clueless that you don’t realize whether it’s three or five doesn’t matter? Billy, seriously, sit this one out.

  287. 287
    Daniel King says:

    gpuccio to Cartelli:

    You are not capable of any serious and respectful discussion

    What an arrogant and hostile thing to say!

    ..and your only partial excuse could be that your understanding of biology is really ridiculous.

    You should be ashamed of yourself for resorting to such desperate and meaningless ad hominems.

  288. 288
    bill cole says:

    Alicia

    Billy, are you kidding, I said I wasn’t sure if it was three originally. So it’s five. Either way it’s a fraction of what is used by living organisms today. Are you so clueless that you don’t realize whether it’s three or five doesn’t matter? Billy, seriously, sit this one out.

    What is your evidence that it has ever been less than 20? If so how many nucleotides did DNA have in your 5 amino acid world? If still 4 can you explain how having 5 amino acids made RMNS more than a just so story? The argument strategy you are using makes me believe you do not understand the sequential space problem that gpuccio has been trying to educate you on. By saying gpuccio does not understand biology you are losing credibility especially when you thought the NPC was a single binding entity. Alicia, are you capable of debating wo ad homenim put downs?

  289. 289
    bill cole says:

    Alicia
    Do you realize that 3^200 is quite a bit smaller than 5^200. Do you know how much smaller?

  290. 290
    Dr JDD says:

    Alicia – why are you being dishonest here?

    All they demonstrated was that to make a beta-barrel like fold that could bind saturating amounts of proline rich peptides immobilised on beads (low hanging fruit for “function”) they could get away with replacing most of the 57 amino acids with a reduced amino acid of 5 (rather than 20).

    Additionally of those 57 amino acids, 12 were not attempted to be simplified!!! Presumably because all function and/or folding was lost. Further, of the remaining, at least 4-5 for each variant they discuss did not tolerate a reduced amino acid substitution.

    Finally, let me reiterate that this was an SH3 domain of src protein. It is not a protein of any use itself, simply a proline binding domain of a larger functional protein. And as already stated, to get a structural feature is not that difficult (beta-barrel like fold) and also to bind proline rich peptides (you will know how unique proline is and how is kinks polypeptides and can be easily interacted with by other polypeptides even more so when selected for this binding by immobilising a high concentration of proline rich polypeptides on beads), but how is this a “functional protein” of any use in a cellular organism?

    And again, I come back to my original question – why did they not insert these reduced aa mutants back into the context of the whole src protein and demonstrate the functionality of that protein was maintained?

    This paper does not support your assertion and you are dishonest if you continue to suggest it does!

  291. 291
    Dr JDD says:

    Gpuccio:

    If you want access to this article go to academia.edu (or google the full title of the article and it will be one of the top hits) and you can create an account as someone with an interest in the science and get access to the pdf.

    I recommend it – it is an interesting paper.

  292. 292
    Dr JDD says:

    I think it would be helpful to outline the findings of the paper from Baker’s lab that Alicia says that she cites almost every time she is at UD. Bear in mind this citation is supposed to support the assertion that functional protein sequences are highly common and therefore this vastly reduces the search space for a given sequence. It is also supposed to support the notion that most amino acids in a given protein are mutatable which is also seen as support for many solutions to a functional problem with regards to protein sequence.

    I should note here whilst I agree with the thought that “perfectly optimised function” is not necessary (i.e. a reduced function over the “final” wild type sequence can be sufficient), this reduced function has to be physiological. In other words, if an enzyme can still catalyse a reaction but this now takes 12 hours instead of 12 seconds, you have a problem if the product of that reaction is indeed necessary to support a particular cellular role necessary to life/survival. Further to this, physiological relevance extends not only in efficiency but in other parameters such as affinity/concentration (i.e. there needs to be enough of the substrate around for the affinity of the protein for that substrate, so physiological levels, not supraphysiological levels) and also the needs of the system as a whole and the properties the sequence invokes.

    Good examples of the last point are things like protease susceptibility, degradation/turnover rates, etc. Further, the environment can play a role. A good example of this are thermophilic bacteria where the most “optimal” enzyme or protein sequence may not be the most efficient – in fact it is highly unlikely to be the most efficient, but rather, it will be the most efficient in the context of being able to function at say 70-90oC (i.e. thermostability is a driving factor here).

    Now I am not saying those things cannot come about through RM+NS (especially thermophilic bacteria), however I would personally suggest that the starting point could not have come around through RM+NS (in other words, a thermophile may have arisen through RM+NS from an ancestor that did not possess thermophilic enzymes. Possibly.).

    So, let’s return to the citation at hand and try to see if this supports the original assertion.

    In this paper, the researchers tried to see if they could use a simplified amino acid output (instead of the full 20 common amino acids found in most life today) to make a domain of a functional protein. This is an important note, as they simply are looking at the SH3 domain of the src protein. This domain is not a “functional protein” in the sense of on its own in the cell serving a cellular function. It is a domain of the src protein that binds to proline rich sequences. Proline is an amino acid that is perhaps the most unusual one as it provides less flexibility in polypeptides that make up proteins, and induces structural features such as “kinks”. It has a (non-aromatic) ring-like sidechain to achieve this. It is known that proline-rich repeats form helical-like polypeptides with good features for other proteins to interact with.

    The authors state:

    The SH3 domain has a complex beta-barrel-like structure wherein residues spread throughout the sequence come together to create the binding site for a proline-rich peptide. Because peptide binding requires proper folding of the SH3 domain, selection for binding activity necessarily selects for the SH3 fold.

    In order to achieve this, they used phage display combinatorial libraries (which can allow for the assessment of many millions of different mutants). To isolate those mutants that passed the criteria they panned the phage with paramagnetic beads that were coated with proline rich peptides.

    Now here is a very important point that they make (remember, this is about the 57-amino acid SH3 domain from the src protein, not about the src protein itself, which is about 535 amino acids):

    Combinatorial libraries of SH3 variants displayed on the surface of M13 phage were constructed in which all residues not involved in binding were biased towards a small set of amino acids. [emphasis JDD]

    That is a very important point, which we will come back to.
    Next, what reduced amino acid set could they use? They attempted to use one nonpolar and two nonpolar amino acids (based on cooperatively folded helical structures obtained from random sequences predominantly were composed of these as they cite) however this 3-amino acid alphabet did not work. What they found was that the majority of the Alanine (A) and Glycines (G) in the wild type sequence could not be replaced, so they included these 2 with Isoleucine (I), lysine (K) and glutamate (E). These are then the 5 amino acids they used.

    Next, another important statement the authors make:

    At positions where structural and phylogenetic data suggested that one of the reduced alphabet residues might not be tolerated, additional residues were included…

    Having performed the technical work, they had a large number of hits but for obvious reasons could only check a limited number had properly folded. However, these libraries were performed I believe in 3 segments across the protein domain and then had to be stitched together. At the splicing sites further simplification was attempted, and 2 variants came through this process (FP1 and FP2). FP2 was the most simplified variant, and 40 of the 45 residues attempted to be simplified had been simplified.

    But remember – the original SH3 domain was 57 amino acids. So where did the 45 come from? Well, as stated earlier, they only mutated those residues not involved in binding! So 12 of the 57 were deemed critical for proline-rich peptide binding. Then out of the remaining (presumably providing mainly structural characteristics to form the beta-barrel), they managed to get 40 to be simplified. The 95% number already discussed in this thread then comes from this statement:

    Three of the five positions that resisted simplification are at or near the binding site; the protein scaffold that supports the binding site is 95% I, K, E, A, and G.

    That is a bit different from claiming 95% of amino acids in a protein can tolerate change.

    Now to be fair, the authors do address the 12 non-mutated binding residues:

    Since there are exposed large hydrophobic residues at the binding site that may compromise stability, further simplification could likely be achieved if the requirement for binding were relaxed. For example, of the 12 positions held fixed in this study, half were shown to tolerate alanine substitutions in the Sm5 SH3 domain; judging from the effects on expression levels, only one of these mutants appeared to have significantly reduced stability.

    Now this is surprising, as if they could have truly mutated those residues along with other simplification of residues not involved in proline-recognition, this would have been a much greater impact and story to tell. Yet they have not published anything of the sort, but simply reference a paper that individually mutates a residue to an A at a time to determine critical residues. This is a far cry from mass mutation and I do think it is telling that they have not done this themselves (which usually means they did it but it did not work).

    The authors go on to characterise some of the structural features and states of these variants they have produced, but I am not sure how important it is to go into detail as I think the above spells out quite clearly that what this paper was being cited to show, is emphatically not what it demonstrates.

    So a reflection point here:
    – Does this paper support the assertion that whole functional proteins can retain biologically relevant function when the vast majority of their amino acids are simplified to a 5-letter aa alphabet?
    – Does this paper support the assertion that 95% of a protein’s residues are mutatable?
    – In the last 20 years, is this the best support of the above assertions? Where are the papers looking at simplifying, say, ATP synthase or something fundamental to most of life from the simplest form known?
    – Who do you think is really being honest here?

  293. 293
    gpuccio says:

    Daniel King:

    “You should be ashamed of yourself for resorting to such desperate and meaningless ad hominems.”

    No ad hominem. Just an explicit judgment about Alicia’s moral character, as expressed in her management of the discussion here. A judgment of which I take full responsibility, and on which of course you are free to disagree.

    As you are free to give similar judgments about my moral character as expressed in my discussions here.

  294. 294
    gpuccio says:

    Dr JDD:

    Thank you for you kind advice at #291. I got the full article! 🙂

    And above all, thank you for your competent, balanced and fascinating comments at #290 and #292. I fully agree with what you say.

    This is another kind of paper which says interesting things, but draws inappropriate conclusions from those things, regarding supposed evolutionary implications. We can be grateful for the interesting work, but there is no need to share the conclusions.

    What we certainly do not need to share are Alicia’s “conclusions” from the paper, which are well beyond reason and honesty!

    Thank you again.

  295. 295
    Mung says:

    Alicia provides entertainment for free! Let’s not be too harsh with her.

  296. 296
    Dr JDD says:

    Thanks for your comments gpuccio – and good to see that you share my thoughts on the results presented in that paper.

    Mung – I agree as well I am not one to hang one out to dry nor am I one to dish out the ad hominems intentionally (even though Alicia has said many negative things to me in the past). I am happy to withdraw my assessment of Alicia as being intentionally dishonest if Alicia can either demonstrate emphatically that there is a misunderstanding of these results or state that she herself was wrong and misinterpreted the results to state something that this work does not support.

    I sincerely believe that gpuccio is correct and our understanding of this paper emphatically does not support the assertions made about tolerance of mutations in general and/or available sequence space. Also we must consider the biological context and not just “something has limited function”. This is essential as I believe gpuccio has well laid out here with the example of STAT3 – and there are many other examples of large proteins that show little to no variation as you look across the species. The question remains – how did RM+NS arrive to such a sequence when it is clear it is so important.

    The assertion Alicia is making that it shows this is the most optimal sequence and it matters so after millions of years it arrives at that optimal sequence and doesn’t change – this is completely ad hoc. There is no evidence to support that, unless one can show a route that the STAT3 could have taken or at least simpler predecessor molecules. This is therefore no different to saying “goddidit” but somehow it seems acceptable to then slate and claim that someone does not understand basic biology for not accepting this “just-so” story (that lacks any evidence to support it).

  297. 297
    bill cole says:

    Dr JDD
    Thanks you very much for going through the paper in detail.

    I agree with Mung that we should not gang up on Alicia despite her frequent use of put downs and odhominem attacks.

    She is often supporting a minority opinion of this blog and I know how difficult this can be.

    The sequential space problem is real and there are not any solutions yet that have delivered a mechanism that can generate new genetic sequences.

    The counter argument is that these sequences started out as simple and then through natural selection became more complex. No one has come close to modeling this without a target (knowing the sequence and comparing the mutated change to the final working sequence)

    The closest is a reference Dr Joe Felsenstein gave to me in a discussion on the Sandwalk blog.

    But check out the simulations of Karl Sims, or the program breve that enables you to simulate a similar case, or the Boxcar2d system which does something similar (I have left out links because these are easy to find using a browser).

    I would be interested in your opinion if you think this simulation shows the ability to generate primitive genetic sequences.

    Whether it is 20AA or 5AA in the sequence random change will degrade it. I understand Alicia’s frustration trying to defend the existence of a valid evolutionary mechanism given the genome is a sequence. Sequences are great at creating diversity but suck at trying to create them with a random search (their use as a password is an example) Passwords are designed to block random search. Some are only 4 digits long i.e. ATM passwords and do a good job securing your bank account.

  298. 298
    Dr JDD says:

    Hi Bill,

    I am certainly no expert on simulations or codes nor modeling evolution. I may claim to have some expertise on understanding what phage libraries can do, biological relevance of protein function, cell biology systems, etc, but what I state above is just using my knowledge as a scientist combined with the ability to critically read a published piece of work. But you do not need to be a scientist or have done that for decades to be able to do so as other hear prove.

    It seems to me though that simulations that use other systems are pitiful for trying to understand these things. They work with 1 goal in mind typically and this is dreadfully inaccurate for biological systems. For example, as you mention it see:

    http://boxcar2d.com/

    It seems to me you are simply trying to evolve a car to travel the furthest. But notice some key features, for example, you need a wheel, it needs to turn…the path is defined, the number of shapes and objects are very limited, etc, etc. However, it is 1-dimensional in its goal – travel the furthest.

    Now take for example a living organism. It requires the ability to replicate, and survive to a point of replication. But to achieve the utilization of energy, replicating in a way that information (!) is passed on and retained. Even at the simplest point, this is multifactorial.

    This is where the discussions of individual proteins really could not convince me even if you can show a “simplified” version of the protein. The point is biologically speaking it is not about 1 protein. If it accumulates too much, it is toxic to the cell. If it interacts with the wrong thing too much, it can be toxic to the cell. If it is not good enough for the substrates relative biological concentration, it is of little use. Just because you can create in isolation or even simulate a simplified version of a protein or a pathway to a more complex protein from a simple one, does not mean it would work in a biological multi-factorial system. And earlier on in evolution, there would have likely to have been less redundancy so such pathways are even harder to achieve.

    That is why I come back to the point I made above – why didn’t they put some of these “simpler” SH3 domains into the src protein and show functionality. If they cannot even do that, how can you even maintain this is a rational path for the evolution of a protein. There is a reason they have a more complex amino acid composition – undoubtedly it is required under the constrains of the biological system.

    However the truth still remains that these simulations and other attempts to model protein evolution from simple to present day observations have all woefully failed. Therefore, it is all hear-say, just-so stories and ad hoc reasoning with no sound basis except a good imagination.

  299. 299
    gpuccio says:

    Dr JDD and Bill Cole:

    Thank you for your always interesting comments. I would like to add a few thoughts:

    1) Regarding Alicia, I can appreciate (her?) for a short time, and sometimes I have found some interesting points in her posts. But in time she becomes unbearable, and most times uses the most arrogant and pointless arguments as though they were absolute truth that everybody should revere. So, I will go on with my mixed feeling (and behaviours) with this person.

    2) Regarding optimal or suboptimal function. The point is simple: in the proteome we find a lot of function, nobody can really say if it is optimal or not, but certainly it seems to work very well. Let’s remember that in the famous rugged landscape paper (Hayashi) the wildtype could not be found by experimental means, and only highly suboptimal solutions emerged, none of which was a path to the wildtype.

    So, let’s say that Stat 3 gains its 1000+ bits of functional information in cartilaginous and bony fish, and that those 1000+ bits are conserved to humans, for 400+ million years.

    OK, I suppose Alicia would say that those 1000+ bits are some optimal information and that’s the reason they are conserved. OK, let’s say that is the case.

    The question remains: how did those 1000+ bits of optimal functional information appear?

    The answer of darwinists (including Alicia) is always the same: it came through gradual evolution, by RV + NS.

    But where is the evidence for that? In their minds, and nowhere else.

    Facts:

    a)In the genome – proteome there is no trace of any intermediate sequence between the proteins which existed before vertebrates, and the protein which we find today in the oldest vertebrates (sharks). There is, instead, this amazing conservation between sharks and humans (and everything else in between).

    b) Similarly, there is absolutely no evidence of any “suboptimal” form of the Stat 3 protein (or of any other similar case) which could represent at the same time an intermediate function and an intermediate sequence. IOWs, what the darwinist theory badly needs and never finds.

    c) Any hypothetical suboptimal intermediate should have been functional enough to confer some reproductive advantage in its due time, so that it could expand and be fixed. That’s the only way intermediates can help. IOWs, each intermediate must have been under real positive selection, in its due time. But, for some strange reason, there is no trace of those processes.

    d) In all that we can observe, we see constant evidence of negative selection, IOWs conservation of functional information which already exists, or just the emergence of new blocks of information, be them new genes, or new parts of a gene, or simply functional modifications of existing genes, always with definite discrete functional jumps, some of them smaller, some of them really amazing. And any jump above, say, 120 bits is well beyond the probabilistic resources of our whole biological planet.

    e) What can never be seen is positive selection which generates new complex functional information, as documented by definite paths where gradual suboptimal states are capable of being naturally selected and expanded, and are at the same time sequence steps to the final “optimal” state. There is no trace of that, IOWs, of the mechanism itself which should explain everything in the mind of darwinists.

    f) So, the observable facts are: a proteome which is full of evidence of the sudden appearance of new information, of the conservation of existing information by negative selection, and of the modification of what can be modified by neutral variation, without any functional consequence. IOWs, a proteome which screams design and conservation of design, while wholly falsifies the “theory” of gradual paths to complex functional information.

    So, the final question is: what shall we follow, observable facts and good reason, or Alicia’s personal fantasies?

  300. 300
    bill cole says:

    Dr JDD
    Thanks you for your thoughts. I have come to a similar conclusion. Although Joe has come pointed me to a very clever model of population genetics it does not explain the evolution of new features like GPS that are mission critical to the journey through common ancestor theory. As your point articulates it is single dimensional.

    GPS ( or a genetic equivalent like wings) require new genetic sequences of which we have no known mechanism for generating.

  301. 301
    bill cole says:

    Hi Gpuccio

    d) In all that we can observe, we see constant evidence of negative selection, IOWs conservation of functional information which already exists, or just the emergence of new blocks of information, be them new genes, or new parts of a gene, or simply functional modifications of existing genes, always with definite discrete functional jumps, some of them smaller, some of them really amazing. And any jump above, say, 120 bits is well beyond the probabilistic resources of our whole biological planet.

    This statement is absolutely valid but not always easy for biologists to see. Even those with valid PHD degrees from major universities can struggle with this concept based on the almost infinite sequential space of the genome. I have seen a few who are not completely tied to certain world views come around after months of rigorous debate. I participate on a few blogs where Alicia’s opinion is the majority and see some progress in participants understanding the problems with current evolutionary mechanisms like RMNS neutral theory etc. Bottom line this is very obvious to you me and Dr. JDD but takes time for others to see clearly. This topic was first brought in the Wistar conference in 1967 and is still being debated 50 years later.

  302. 302
    Dionisio says:

    gpuccio @299

    […] in the proteome we find a lot of function, nobody can really say if it is optimal or not, but certainly it seems to work very well.

    Good point.

    The question remains: how did those 1000+ bits of optimal functional information appear?

    Good question.

  303. 303
    Alicia Cartelli says:

    As usual pucci, all of your “facts” are wrong.
    Just because you are incapable of both literature searches and learning new information, this does not mean that the information is not out there.
    We have learned a lot about protein evolution during the last 50 years of research and there is much evidence for it.
    Again, try a simple pubmed search and you will find an avalanche of papers on the evolutionary history of many protein families.
    Maybe you’ll even learn something, who knows.

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