1,177 human orphan genes removed by evolutionists from databases
| April 13, 2014 | Posted by scordova under News |
Here is a case of evolutionary bias causing misrecognition of orphan genes in humans. Orphan genes are presumed protein coding genes that exist in only one species and have such non-similarity to anything in any other species they are called orphans (a play on words of the ORF acroym for Open Reading Frame).
This came up in the Nelson-Velasco debate where Velasco said there are 0 orphan genes, and Nelson pointed out the reason some say they are zero is because of their biases.
Nelson has been vindicated as I pointed out in New Mechanism of Evouion — POOF
Here’s is the proof of this cover up Distinguishing protein-coding and noncoding genes in the human genome:
1. “The remaining 1,177 cases were declared to be orphans, because they lack orthology, paralogy, or homology to known genes and are not obvious artifacts… If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes… We found… 12 reported cases of orphans with experimental evidence for an encoded protein”
The problem with these authors is in 2007 they didn’t invoke the POOF mechanism of evolution which other evolutionists happily embrace now in 2013:
However, with the advent of sequencing of full genomes, it became clear that approximately 20–40% of the identified genes could not be associated with a gene family that was known before. Such genes were originally called ‘orphan’ genes
20-40% of the genes discovered cannot be explained by common ancestry or common descent. So what mechanism is left to explain it? Special creation? But evolutionists can’t accept special creation, so they just pretend they’ve made a discovery of a new mechanism of evolution that can work just as well.
They haven’t given it a name yet, so let us call it POOF. What is POOF? POOF is the mechanism by which proteins can easily arise out random nucleotide sequences like a poem can emerge out of randomly tossed scrabble letters. I bold one of their euphemisms for the POOF mechanism in the following paragraph:
Orphan genes may have played key roles in generating lineage specific adaptations and could be a continuous source of evolutionary novelties. Their existence suggests that functional ribonucleic acids (RNAs) and proteins can relatively easily arise out of random nucleotide sequences, although these processes still need to be experimentally explored.
😯
The reasoning they use goes like this, “we have all these genes that can’t be explained by slight successive modifications, so they must have arisen spontaneously out of nowhere. Because evolution is fact, this implies evolution can just take random material and create functional systems in a flash. We’ve made a fabulous discovery about the miracles of evolution even though we can’t demonstrate it experimentally.”
HT JoeCoder
www.reddit.com/r/creation
128 Responses to 1,177 human orphan genes removed by evolutionists from databases
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Remind me again! how the following two claims are consistent:
1. Chimps, Humans 96 Percent the Same, Gene Study Finds, and
2. 20–40% of the identified genes could not be associated with a gene family that was known before (Tautz et al above)
What in heaven’s name is going on??!?
Salvador claims to be in favor of a self-correcting community. He whines when he receives abuse for disagreeing with ID.
So why does he delete posts which expose his ignorance?
Salvador:
No, Sal, that’s not what an orphan gene is.
Here’s the link to the Wikipedia article.
Here’s how the Discovery Institute defines them:
And there’s this:
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan genes is mistaken?
I think not.
Mung, I am confused. You present three definitions for an orphan gene. To my layman’s eye, all three are substantially the same. So what’s your point?
Moose Dr,
The point is that none of them agree with Salvador’s definition!
Have you noticed that Salvador deletes my posts? If he has nothing to fear from the truth, why would he do that?
Its interesting when you read the linked material, rather than accepting the interpretation. If I understand the article correctly, when human DNA is searched for the “start code” (ORF) a total of 1177 orphan (non-homologous ORF) cases are found. However, specific proteins produced from those orfs are not detected.
This report does not seem to present a fresh experiment to find the proteins associated with these orphans. However it reports that twelve such proteins are reported in the literature.
Their argument seems to be that the digital detection of an orphan means little, that the second step of detecting that the orphan actually produces a protein is called for.
I don’t find their case unreasonable. I think it important to understand how many true protein-coding orphans there are. What is clear is that there hasn’t been a search for a matching protein in all 1177 cases of orphans. So the orphan count is likely to climb to much higher than the mathematically impossible 12.
One of the challenges is that certain proteins may be expressed only in certain stages of development and some only under environmental stress or other specialized conditions.
That is why I said the orphans are presumed to code for proteins. We don’t know for sure.
The point is, it is distressing they’ll just force the evolutionary paradigm and shut down inquiry. What is there to lose if they are really orphans? A lot. What is there to lose if they aren’t? Nothing.
Thus to me, the 2007 paper symbolizes an attitude that is bad for science. The 2013 paper symbolizes a more open view.
scordova:
Does anything shut down inquiry like deleting the posts of dissenting opinions?
Salvador:
From the DI web page on orphan genes:
Salvador is as young earth creationist.
Right Sal?
Or are you riding the fence on that as well?
Moose Dr,
The point is that none of them agree with Salvador’s definition!
Have you noticed that Salvador deletes my posts? If he has nothing to fear from the truth, why would he do that?
A more important challenge is to find someone who is honest.
Moose Dr,
The point is that none of them agree with Salvador’s definition!
Have you noticed that Salvador deletes my posts? If he has nothing to fear from the truth, why would he do that?
Meanwhile, Salvador, the champion of dissent, deletes dissenting posts from his threads.
The deleted materiel:
Salvador deletes my posts because he’s a hypocrite who doesn’t care for the truth. What’s good for the goose isn’t good for the gander.
Salvador:
No, Sal, that’s not what an orphan gene is.
Here’s the link to the Wikipedia article.
Here’s how the Discovery Institute defines them:
And there’s this:
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan genes is mistaken?
If I understand this right (and I should qualify that I’m far from an expert), there are actually two different things contributing to the apparent discrepancy.
First, most (/all) of the orphan genes are very very similar to non-protien-coding regions in related species. Thus, new genes can be produced with very little (percentage) change in the DNA sequence. For some examples, take a look at “Recent de novo origin of human protein-coding genes” by David G. Knowles and Aoife McLysaght in Genome Research 2009. 19: 1752-1759 (I happen to have it handy because I cited it in another thread…). It examines three novel genes found in humans but not other primates, and examines the changes that produced them in detail. Specifically, look at part B of figures 2, 3, and 4 — they give the full DNA sequence for the genes in humans, compared to the syntenic sections of the chimp and macaque monkey genomes. In the first one (the CLLU1 gene, figure 2), the full sequence is 369 bases (including the human start and stop codons), but I count only 8 single-base differences (just over a 2% difference). Note that only one of those was responsible for the change:
The other two novel genes are a bit more different (in the last case, the human sequence actually has a 10-base insertion), but they’re still pretty similar to the other sequences.
The second factor is that (if I understand it right) the 20-40% figure refers to all genes across many species, not the genes in a single species. To see the importance of this, consider a (hopelessly oversimplified and unrealistic) example. Suppose we’ve sequenced a thousand species, and we found two thousand genes genes shared by all of the species, and that each species also has a single gene that’s unique to that species. This means that there are three thousand genes total, and 33% of them are “orphan” genes. But for each individual species, only one of its 2001 genes is an “orphan”, which is just 0.05%. Reality, of course, is much more complex and messy than that. But hopefully it illustrates the point…
“One of the challenges is that certain proteins may be expressed only in certain stages of development and some only under environmental stress or other specialized conditions.”
A valid point.
“The point is, it is distressing they’ll just force the evolutionary paradigm and shut down inquiry.”
I don’t see them shutting down inquiry. They seem to want to keep orphans out of the gene databases until a protein is verified. This position should spur exploration into the 1177 to find produced proteins. At least hopefully.
“What is there to lose if they aren’t? Nothing.” The paper’s authors argue exactly the opposite. They suggest that putting genes into the gene database will cause researchers to focus on irrelevant data.
I have to agree with Moose here; they aren’t trying to shut anything down, just recommending updating the annotations based on additional information. Sequence annotation — basically, picking out and labeling the interesting bits of the genome — is a very approximate science at this point. If those 1,177 “genes” are removed from the gene catalog, it doesn’t mean they’re being censored, just that our “best guess about what they are” is being downgraded. They’ll still be in the actual full genome data, and since the annotations are approximate (and everyone knows it), they’ll still be reassessed and re-reassessed and… Some will probably be removed from the catalog and re-added and re-removed and re-re-…
Ian Thompson @1:
Somebody is lying, of course, hoping that nobody notices the obvious BS.
Moose Dr,
The point is that none of them agree with Salvador’s definition!
Have you noticed that Salvador deletes my posts? If he has nothing to fear from the truth, why would he do that?
Meanwhile, Salvador, the champion of dissent, deletes dissenting posts from his threads.
The deleted materiel:
Salvador deletes my posts because he’s a hypocrite who doesn’t care for the truth. What’s good for the goose isn’t good for the gander!
Salvador:
No, Sal, that’s not what an orphan gene is.
Here’s the link to the Wikipedia article.
Here’s how the Discovery Institute defines them:
And there’s this:
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan gene is mistaken?
Meanwhile, Salvador, the champion of dissent, deletes dissenting posts from his threads.
The deleted materiel:
Salvador deletes my posts because he’s a hypocrite who doesn’t care for the truth. What’s good for the goose isn’t good for the gander.
Salvador:
No, Sal, that’s not what an orphan gene is.
Here’s the link to the Wikipedia article.
Here’s how the Discovery Institute defines them:
And there’s this:
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan genes is mistaken?
Meanwhile, Salvador, the champion of dissent, deletes dissenting posts from his threads.
The deleted materiel:
Salvador deletes my posts because he’s a hypocrite who doesn’t care for the truth. What’s good for the goose isn’t good for the gander.
Salvador:
No, Sal, that’s not what an orphan gene is.
Here’s the link to the Wikipedia article.
Here’s how the Discovery Institute defines them:
And there’s this:
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan genes is mistaken?
Moose Dr,
The point is that none of them agree with Salvador’s definition!
Have you noticed that Salvador deletes my posts? If he has nothing to fear from the truth, why would he do that?
Moose Dr at #3:
When an ORF is detected in a genome, it happens very often that no protein has been found that corresponds to the ORF. Protein detection is a much more difficult process than ORF detection at the genome level. The authors of the paper are well aware of that, when they write:
Therefore, their argument is not that proteins have not been found (that would invalidate a lot of ORFs in most genomes).
Their argument is simply that those 1177 ORFs cannot be explained according to a neo darwinian model. That’s very clear in their final conclusion:
Emphasis mine.
Now, I have no ides if those ORFs are really protein coding genes or not. However, it is very clear that the only reason why they have been considered non coding is that they cannot be easily explained by a neo darwinian mechanism.
I am fully confident, however, that if and when 1177 proteins corresponding to those genes will be found, demonstrating that they are indeed protein coding genes, a darwinian explanation for that will immediately be found 🙂
Mung, so what? The difference isn’t significant to the discussion.
Matzke was an early orphan denier. According to him, back in 2006, orphans would disappear with enough sequencing.
It looks like Nelson was right and Matzke was wrong, orphans are here to stay.
Jehu:
Fine. Salvador is God.
My bad. Dr. Salvador. Senior Engineer.
Gordon Davisson at #5:
The 20-40% figure is just a reference to the percentage of new genes that can be considered as orphan genes in all genomes. That is clear at the beginning of the Tautz paper:
So, that has nothing to do with the specific case of human orphans. In the case og human genome, 1177 (carefully reviewed orphans) out of about 24000 (original ORFs) would be about 4%, so still lower than the general case.
Your discussion about new genes arising from non coding segments is extremely important, but I think it has nothing to do with the 1177 orphans, for which, if I understand well, no homology has been found in other genomes, even in non coding parts (that is exactly part of the argument in that paper).
The problem remains:
a) either they are non coding segments (and they could be non functional, or functionla, like all non coding segments)
or
b) they are true protein coding genes that cannot be explained by any neo darwinain model.
I suppose that truth is probably a mix of the two.
Regarding, instead, new functional genes that arise from non coding segments, that’s a very important observation, already proven in a few cases, as you correctly explain. It’s also, IMO, one of the strongest arguments for design. I strongly believe that many new functional genes are gradually designed from non coding segments, probably mainly through guided transposon activity, and “released” as functional genes only if and when it is necessary. I have argued in that sense many times here.
So they have gone from Matzke’s argument that enough sequencing will find the parents to the argument that the orphans do not code for anything.
It looks like VJ Torley was right and Salvador was wrong.
Jehu:
Jehu, be fair! Remember that it’s easy to be right defending a right theory. Everybody is good at that!
Let’s give Matze full merit in trying to defend as well as possible a wrong theory. 🙂
In other words, they have gone from being orphan “deniers” to junk DNA “truthers.” LOL.
Jehu:
Obviously. Do you remember the good old Sherlock?:
“How often have I said to you that when you have eliminated the impossible (IOWs, that neo darwinism may be wrong 🙂 ), whatever remains, however improbable, must be the truth?”
To all:
I suppose that a good question would be the following one:
Is this situation unique of the human genome, or not?
IOWs, how many orphans are there in, say, the dog genome, and how many of them would be discarded as random non coding sequences according to the methodology used in that paper?
Salvador deletes my posts, regardless of their content. He claims to support self-correction, but that only seems to be the case when correction applies to someone else.
Salvador:
No, Sal, that’s not what an orphan gene is.
Here’s the link to the Wikipedia article.
Here’s how the Discovery Institute defines them:
And there’s this:
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan genes is mistaken?
Salvador:
No, Sal, that’s not what an orphan gene is.
Here’s the link to the Wikipedia article.
Here’s how the Discovery Institute defines them:
And there’s this:
Does it even makes sense to launch into a discussion of orphan genes if what constitutes an orphan genes is mistaken?
Are you a Christian Sal? At times I really wonder.
RE #6 (Moose D=r) –I would personally have to somewhat disagree with this:
The reason I disagree is from a practical experience point. When I have done risk analyses by BLAST searching the human genome for short peptides of a specific length (to assess risk of a protein we have made to detect this peptide), we often come across many proteins that when you try to design primers and find tissues where it is expressed, you have trouble. When you trace it back and look at the data it is most likely an ORF that is a predicted protein. There are 100s of these in the human databases that we use, that have no “evidence of protein” available yet in the literature, yet they are still included on the hit list (and not relegated further down the list of priority, just because there is no evidence of actual protein translated from this sequence).
Therefore despite me not being a geneticist and rather a cell biologist, I would conclude that there are in fact many ORFs with no evidence of protein from these yet they are included in databases that most scientists use. As such, I cannot agree that there practically is a drive to “keep orphans out of the gene databases until a protein is verified” as this is not what I personally experience on a day to day basis. Although I can admit, I may be wrong in that there is some other evidence besides what is listed there (protein evidence or lack of) for its inclusion in these databases, but this is not how it appears, and to quote my colleagues in the relevant department when I ask if this is a real risk, “This probably is a gene that does not exist as a protein” (therefore they take it as a hypothetical ORF that is present in the database).
We would be good to remember though that as pointed out here, lack of evidence at this stage could be due to lack of understanding the right conditions and mechanism for expression of said ORF into a real protein (much like the junk DNA theory commonly subscribed to 10 years ago).
JD
Dr. JDD,
Actually authors of the preceding ‘kick the ORFans out in the street’ paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias:
http://www.uncommondescent.com.....ent-358547
Dr JDD:
I absolutely agree with you, and I have erxpressed similar ideas in posts 25 and 30.
I would add that, in this particular case, given the huge phenotypical differences between humans and chimps, and the minor differences in known protein coding genes, which can scarcely begin to explain those differences, it should be the primary duty of researchers to concentrate on DNA differences between the two species.
1177 potentially protein coding sequences which are completely new should really be at the center of attention, not to deny their importance, but rather to verify their functional meaning. Even if they were not protein coding genes, they could just the same be regulatory genes. However, they should be thoroughly investigated.
Instead, what do we see? Academic scientists do their best to simply deny their importance and to delete them from the ORF database. And how do they do that? Simply showing that, if they were really protein coding genes, their personal model (neo darwinism) could not explain them.
For me, this is cognitive bias at its worst.
BA:
Thank you for linking to that old post of mine. I think it remains valid. They simply want to interpret those ORFs as arising from coding gene regions, instead of just thinking that they could be coding genes. Pure bias.
Gpuccio I completely agree with you and your previous posts on the matter. I was also just trying to bring a practical example to the table as I think it is useful to see this us a day-to-day observation in practical science as opposed to something just spoken of in a paper and published (very often the two do not converge as we would hope or expect!).
Thanks,
JD
Gpuccio, perhaps several thousand genes could be ORFans given the >39% of orphan enzymatic activities of humans. (Or else alternative splicing is far more radical than previously envisioned)
Orphan enzymes could be an unexplored reservoir of new drug targets. – 2006
Excerpt: Despite the immense progress of genomics, and the current availability of several hundreds of thousands of amino acid sequences, >39% of well-defined enzyme activities (as represented by enzyme commission, EC, numbers) are not associated with any sequence.
http://www.ncbi.nlm.nih.gov/pubmed/16580971
It would be very helpful if one of the authors made a detailed OP on the different issues with genes, coding regions, orphan genes, expressed proteins, origins of the coding regions, etc.
I am under the impression that the neutral theory which has received a large number of posts and comments here lately is essentially a side issue in the evolution debate and that the origin of new genes/alleles and their corresponding coding of new proteins is where the real debate lies.
So a lot of meaningless comments get made on issues which are either not very relevant or which no ones knows much about. Thus, an OP on this might eliminate a lot of the fog which surrounds these and related topics.
And as an addendum to this, a discussion on those regions that seem to be conserved across species and over time within a species would be appropriate since conserved regions means that these regions are selected for and thus preserved and thus have a necessary function. Otherwise the famous engines of mutation would drive them apart within any population and and most certainly across species.
Would be enlightening and eliminate a lot of wasted pixels.
In my previous post above I am questioning the usefulness of the neutral theory of evolution as having any meaningful effect on evolution. In one of Dr. Torley’s posts, there was a map of human migration across the globe
http://www.uncommondescent.com.....sor-moran/
In it one of the most isolated populations on the planet were the inhabitants of Australia which first went there 50,000 years ago. That represents about 1800-2000 generations. So we have the perfect natural experiment. There must be a lot of different fixed mutations in this population than are in say, African or Western European genomes.
So someone should do the research and settle the question.
Having lost all arguments, creationists are now trying to hold on to their last strand of hope – ORFans. Almost every other post by Vincent Torley and Sal Cordova mentions them!
But there’s no hope for creationists here too.
I had, in fact, pointed out in one of Vincent Torley’s threads a few new studies showing how de Novo gene synthesis happens from non-coding DNA. Curiously he seems to have ignored all the evidence and keeps on repeating science has no idea how ORFans arise.
I’m re-posting papers reporting origin of new genes from intergenic DNA:
1. Emergence of a New Gene from an Intergenic Region (in Mouse)
http://www.sciencedirect.com/s.....2209014754
2. Origin and Spread of de Novo Genes in Drosophila melanogaster Populations
http://www.sciencemag.org/cont.....9.abstract
3. Female fly genomes also populated with de novo genes derived from ancestral sequences
http://phys.org/news/2014-03-f.....-novo.html
It’s clear as broad daylight that ORFans can arise by mutations in intergenic DNA. Sal Cordova & Vincent Torley can continue to express amazement at how that’s possible!
This is an absurd statement. Maybe there should be a new logical fallacy,
Besides, what is meant by the term, “creationist?”
Evolve:
I absolutely agree with you that new genes can arise and do arise from non coding DNA, and I have already stated that in answer to a previous post of yours. That is a very strong argument for design.
The origin of new functional genes from non coding DNA cancels completely the role of NS. So, it is a very strong argument for design.
I don’t think, however, that there is any evidence that all, or most, of the new genes arise from non coding DNA. In the case of human orphan genes, I have found no evidence for that in the quoted articles.
gpuccio,
Wouldn’t NS affect the results of newly expressed functional genes?
-Q
Jerry,
I recommend Behe’s Edge of Evolution as a background primer in how genes may or may not evolve. Most posters here are familiar with the arguments made therein. Read the actual book as most of the reviews flat out lie about the contents.
Jerry,
I’d like to second Jehu’s recommendation.
Please realize that Behe is NOT an anti-evolutionist, but the limits of one of the basic mechanisms of evolution is what he examines based on his research on malaria.
-Q
I was the probably the first one on this site to have read the book and commented on it. I knew instantly the implications of the book.
http://www.uncommondescent.com.....ent-125290
http://www.uncommondescent.com.....ent-125324
I was also one of the first ones on this site to have read the basis of evolution from the naturalist point of view. It is not the neutral theory but mutations of non coding regions that is at the heart of the argument. I will see if I can find the reference. It was something Allen MacNeill advised us to read about 6 years ago. It was in a special issue of a journal on Stephen Gould. That is why Allen pushed real hard on his engines of variation. This all goes back about 6 years ago.
Querius at #52:
Yes. That’s an important point. Even genes that are supposed to evolve by neutral mutations only, like would be the case for genes which derive from non functional sequences (non coding DNA or inactivated gene duplicatins) would require NS at the end of the process, to be expanded and fixed in the population, otherwise they would soon be lost, and all the impossible result against all the probabilistic laws would be for nothing! 🙂
That is a further problem for the impossible model of neutral evolution of function, because in some way it would be necessary that the “evolved” sequence, which by definition has no reason to be translated, not being an ORF, should become translated (in the right quantity, in the right context) as soon as it is “ready”. Otherwise, living cells would be repleted of non functional proteins which are being translated in the long time in which they evolve, so that they may be continuously tested by NS, which is not exactly supported by facts.
See also my posts #58, 72 and 73 in VJ’s thread. “When I am wrong”, here:
http://www.uncommondescent.com.....-im-wrong/
I would like to add, to the papers suggested by Evolve, this important paper about humans:
http://genome.cshlp.org/conten.....2.full.pdf
The abstract:
And look at this important statement in the discussion:
And, finally:
As you can see, even if the neodarwinist bias is constantly trying to obfuscate biological research, there are always good scientists who do their good work. 🙂
Ok, great! As you know, Behe doesn’t rule out other, unnamed mechanisms. He just points out the limitations of mutation.
So, instead of looking for other mechanisms, evolutionists simply attacked Behe. Much easier than doing science.
-Q
Thanks for the explanations and links, gpuccio. I wasn’t aware of the three human-specific genes that you mentioned.
Or, more generously, the neodarwinist paradigm (or idealogical contamination in some cases) has undeniably slowed scientific progress as a result.
-Q
jerry at #55:
The problem, with MacNeill’s “engines of variation”, is simply that either they are guided (and therefore they are tools of design) or they are random, and therefore add nothing to random mutations. RV is the sum of SNP + any other kind of random variation.
A few of those mechanisms could be algorithmic, IOWs adaptive. In that case, they are certainly very complex, and they must be considered as designed algorithms.
In the end, design is the only good explanation for what we observe.
Jerry,
Funny that the post immediately following the one you linked to was from me. Okay, so you get it. It can be extrapolated from Behe’s well supported arguments that all this talk about neutral drift is a non-starter for Darwinist evolution and orphan genes are further damning evidence against the theory. In Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes.~10^20 reproductive events you get two mutational steps. That is it. One neutral, one selected. Darwinism does not have enough creative power in all of geological time to create most these genes.
Please ignore that last post from me. I have no idea how that happened but somehow extra text that I did not type was inserted.
Allen MacNeill recommended a book edited by Elisabeth Vrba and Niles Eldredge titled “Macroevolution: Diversity, Disparity, Contingency”
The first article is titled “Disparity, Adaptation, Exaptation, Bookkeeping, and Contingency at the Genome Level” by Jürgen Brosius. In this article he lays out the basic process that create novel coding areas for new proteins. It is all assertion with no proof but it points to what they are hanging their hat on. It is not the neutral theory.
An aside: Brosius is a low life.
Evolve- Please model blind and unguided processes producing protein coding genes from non-coding DNA. Or admit that the claim is unscientific. Thank you.
Neutral theory is important because it is the one case where the mainstream agrees with IDists and creationists — Natural Selection as a matter of principle has little role in molecular evolution, either origination or maintenance of design. Moran says, “well evidence of selection’s absence is all the junk in the genome”, IDists say “the genome isn’t junk, and neutral theory says all that intricacy can’t be by selection, so it’s by design.”
Gpuccio seems to be the man for the job. 🙂
But that’s a lot for just one post. How about breaking it down to several posts. You might want to articulate what it is you want.
Moran is wrong- junk DNA is not evidence against NS. You would think it would but seeing that it is neither fatal nor detrimental, it doesn’t get eliminated.
That said, NS is still their only alleged “designer mimic”. It just makes the most of the relatively few opportunities.
I have tried and admit that I may not be as clear someone else could be who has a better grasp of the technological terms. But I am also trying to get the logic down also. I have been saying for as long as I have been commenting on this site that the debate is over the origin of new alleles. Does anyone disagree? But what does it mean to say, a new allele?
I wrote a long post on it a few days ago in an attempt to make it clear what is at stake. There are two types of new alleles based on their origin and this is actually a great simplification. Anybody, please correct me I am wrong. There are those alleles that are based on coding regions already there and are just modifications of these coding regions. I believe the neutral theory only applies to these regions. Here an allele can get fixed and now the species has only brown eyes or white fur or some other characteristic that was once variable in the species but now become fixed. This is obviously a simplification since more than SNPs change.
But this is not the real debate. There are alleles that arise some how de novo and I believe they could only come from non coding regions. This is what Allen MacNeill meant when he said Neo Darwinism was dead. He wasn’t endorsing ID as so many thought he might by his statement. No he was advocating a much more complex naturalistic process and this is the basis of the new naturalist evolution thinking. That is why he made a big deal our of his engines of variation. I believe it over 50 now. It does kill Darwin’s ideas and the modern synthesis but does not endorse anything close to ID.
There are regions that do not affect the survival of the organism and thus can mutate away till someday by chance one of them turns into a region if coded can produce a functional protein. Obviously I am leaving all sorts of other areas out such as regulatory regions or epigenetic elements that control organism development or expression of a coding region. It is this latter process of allele formation which is at the heart of the naturalist process of evolution. Which is why I say the neutral theory is irrelevant. How does fixing an already existing allele account for anything meaningful in evolution?
I believe there are testable hypothesis that with the current technology (the ability to map genomes quickly and expensively) that could settle the whole debate. Why, because as these non coding, non regulatory regions mutate, they will leave forensic evidence of their history. If such a thing ever existed as a true junk region turning into a functional protein then is should leave behind in those organisms which never quite reached the point where this region becomes functional a very similar sequence to the ones in those organisms that became functional.
In other words if a species truly has a coding region that does not appear in a similar species then remnants of this coding region should appear in the species that does not have this coding region. It should exist as a non-coding section of DNA. And this is testable. If it doesn’t exist then just how did this coding region arise? They must have existed before a sub-population split off and thus could not inner breed. It takes millions of years to form these de novo coding regions so they should be evident in the other populations before the split happened.
Personally, I think this is mathematically impossible but for de novo coding regions to arise it must have happened in this way and if it did it would leave a trail of dead ends in similar species.
jerry:
As we have discussed here (see post #49 by Evolve, and my posts #51 and 56) there is no doubt that, at least in some cases, new protein coding gene derive from previous non coding regions. Sometimes those non coding regions have a transposon origin.
However, there is at present no indication that this is the general case. Maybe it will be confirmed in many other cases, with time, or maybe not.
The derivation of functional protein coding genes from non coding regions is, as I have stated many times, the best argument for design and for guided variation.
As I have said in my post #59, MacNeill’s list of “engines of variation” is irrelevant at best, ambiguous at worst. It puts together vague and undocumented “mechanisms”, as though they could explain something. They can’t.
Random events are random events, whatever their form. SNPs, indels, translocations, duplications, anything that varies the genome randomly can be described as Random Variation. Classical neo darwinism is well aware of the role of RV, and MacNeill’s list does not ass anything. The crucial point for the emergence of new genes remains:
a) the probabilistic powers of neutral variation (extremely low)
b) the algorithmic role of Natural Selection (really irrelevant)
The neutral theory of evolution has shown that the role of NS is not so important as previously thought. On the other hand, neutralists tend to overemphasize the role of RV, which is irrelevant too. The simple fact is that no complex functional information can be explained out of a design theory.
Other “mechanisms” invoked by MacNeill are ambiguous. They could be interpreted as algorithmic (adaptations guided by an intelligent code already existing in cells, and which incorporates actively new information from the environment), or just as forms of neo Lamarkism / epigenetics (without any detail of how they should work).
Some of them are only vague appeals to undefined principles that nobody has ever shown to exist (what I call neo neo darwinism). Explanatory power: practically non existing.
If we want to reason scientifically, we are always back to the same problem: it is either classical neo darwinism (driven mainly by NS) or design.
And you know quite well what I think about that. 🙂
One way to test for non random variation is run several Lenski type experiments and see if the same point mutation emerges at a frequency higher than predicted by random change.
This is too tough and expensive to do rigorously, and maybe even tougher for other kinds of mutation (indels, whatever). The amount of sequencing needed to establish non-random variation is almost unthinkable in terms of financial cost.
James Shapiro cites some data that suggest some variation is non-random, but pre-programmed. That is certainly easy to believe because many protein isoforms are created in what appears a non-random way.
There are MILLIONS of protein isoforms in humans that come from the 20,000 “gene” sites. If protein isoforms can be made, it is not a stretch to hypothesize “DNA isoforms”, but perhaps we should be grateful the designer isn’t doing too much DNA variation, otherwise it would be even harder than it is for scientists to learn about biology if the genomes were not relatively stable.
I am not sure the naturalist would agree with you. If you can get the Brosius article, read it. He certainly would not. It is in a journal titled, Paleobiology (Paleobiology 31(sp5):1-16. 2005 ).
http://www.bioone.org/doi/abs/.....2.0.CO%3B2
If I was a theist evolutionist, I could claim that this is the process by which evolution can proceed to greater complexity over millions of years. And in that sense was design since it was built into the original cell machinery. But this is not design in the sense that Stephen Meyer is using the term whereby he believes there were insertions of information over time to direct evolution.
The examples you listed in your post are just what I am talking about, where non coding regions somehow turn into functional proteins.
I am not sure Allen MacNeill would agree with you nor would I except to say they were designed into the basic cell in such a way to produce new functional information de novo. If only a couple of MacNeill’s engines of variation produce non coding regions which then could over time turn into functional information then that would support the naturalist point of view.
I have said that this a way to test Axe’s thesis that functional proteins are so rare that such a process could not hope to produce more than a few. Your example of the human protein forming this way may be counter to Axe’s thesis. We would have to get more information on just what happened but it seemed to follow the pattern that I said must exist if this process is viable.
Maybe I read your post wrong but it said there was a coding region in humans which has similar but non-coding regions in other primates and this is heart of the naturalist theory.
I have asked Allen MacNeill to have a dialogue on this and he said he was not against it but it may have to wait till a time he is less busy, maybe at the end of the school year. MacNeill has discussed this briefly in the past on this site. Here is the link:
http://www.uncommondescent.com.....-25by-ago/
Search for both my name and MacNeill and you will find the discussion on this theory, five years ago. There were several others that participated in the discussion and like most threads there are sub-threads that have nothing to do with this concept. Here are two sample quotes from the thread:
http://www.uncommondescent.com.....ent-306698
http://www.uncommondescent.com.....ent-306750
It is these ideas which have to be addressed. That they have been around here several years ago and yet most are not aware of them is something that should be corrected.
This is very long and I hope there are no inconsistencies but if there are they should be corrected.
Two of the links above to Allen MacNeill’s blog were broken. The links to his discussions on variation are:
http://evolutionlist.blogspot......ution.html
http://evolutionlist.blogspot......awman.html
jerry:
I am well aware that “the naturalist” and Allen ManNeill would not agree with me. Indeed, I don’t agree with them. That’s why I am a fully convinced IDist, and they are not.
You say:
.
No, you are wrong. That is not the heart of the naturalist theory. That is simply the heart of a common descent scenario, which I fully accept.
The “heart of the naturalist theory” is that the non coding regions in the primates evolved by mere chance, and that by mere chance they become ORFs and are translated as soon as they are functional.
That is faith in magic. It is not science. The only reasonable explanation for what we observe, and especially for functional proteins arising from non coding segments, is that they are engineered. The only reasonable explanation is design.
The “non coding DNA” -> “functional ORF” scenario is wholly incompatible with NS. It can rely only on mere chance. A “naturalistic” (non design) explanation of that scenario is pure folly.
jerry:
Regarding the probabilistic powers of mere neutral variation, you can maybe look at my posts #58, 72, 73 and 76 in VJ’s thread “When I am wrong”, here:
http://www.uncommondescent.com.....-im-wrong/
I think they “address” in detail the idea you mention, ond of which, believe me, I, like many others, am fully aware.
Wrong about what? Based on lots of conversations/comments/writings in the past here and elsewhere, my statement is accurate.
Common descent from what? Where did these coding sequences arise?
I think you should ask Allen MacNeill about this. I have asked him to comment on this. It is how I read him and his past comments but I could be wrong. It is certainly how Brosius sounds and he was the lead author in the Vrba/Eldredge book highly recommended by MacNeill. There are many naturalist theories. Meyer covers most of them. So you will have to be specific about which one you are objecting to. I believe they all are deficient but I am just presenting what some would say. The example about human and primate coding regions supports their assertions.
They don’t think so and I cannot see any reason why it would be so. NS just acts on variation and the theory in question is about new variation.
The naturalist certainly do not think so. I agree that design is the best explanation but have said they represent testable hypothesis that will solve the debate.
I will read your other comments that you referenced on another thread later in the day when I have more time. But nothing that you said above here changes anything that I said. It seems to reinforce what I have said.
Ok, I read them. I am not going to comment on your calculations. You do not seem to realize that you are preaching to the choir here. I as well aware of the mathematical improbability of generating a new protein. I would remove the word neutral from your discussions because by definition a non coding region is neither positive, negative or neutral. Only when it gets expressed will those characteristics be applicable.
But what you are not explaining is where the various similar coding regions came from in the other primates. Rather then try to interpret your comments, I would ask you to try to explain it better. If you are going to appeal to common descent why do non-coding regions in precursor species suddenly become functional in humans. What is the origin of these precursor DNA sequences?
People like Brosius will say it arose randomly through mutations and at some point a sub-population mutated further till it became functional. I have no idea what Allen MacNeill will say so you should ask him. I have asked him to comment but he comes here sporadically.
I believe the debate will change when these testable hypothesis are researched. And every ORF is testable. It will take lots of time and money but each is getting more favorable each year.
A question and a comment:
Question: It is being repeated here that a portion of non-coding DNA somehow becomes a ‘gene.’ How do we know that?
If the ORPHAN gene is NOT producing a protein—i.e., is not ‘coding’—then how do we know it is NOW a ‘gene’?
Further, if we isolate such ORPHAN genes, then what is the mechanism of the isolation (I admit not having read the 2013 paper—I have absolutely NO time for this right now)?
And, is it being said that the ORPHAN ‘gene’ comes from a “non-coding” portion of DNA because of sequence matching?
I looked through the paper and saw no specific examples, but I’ll presume that they do have such examples.
******************************
My comment is this:
If there is a difference between humans and chimps, then it can’t really be due to little, small differences in the genes that are basically shared between us. We’ve already shown that you’re looking at probably a 1 amino acid difference between their genes and ours; and, this a.a. difference very likely is ‘neutral.’
So, if “de novo” genes are going to make the difference between being a chimp and being a human, then, logically, the genes should be expressed in the very earliest stages of development. If that is the case, then if we are examining chimps and humans that have already been born in determining what proteins are being produced, then these ORPHAN ‘genes’ will show that they have promoter regions and other regulatory regions, but will not produce anything.
It seems logical that if you want to know something about these ORPHAN genes, then you’re going to have to look to early development. And, of course, in the case of humans, this would be highly unethical.
Nevertheless, if there are ORPHAN genes in other species, then the same logic should apply to them, and the activity of these ORPHAN genes can be studied in early embryological stages.
jerry:
Well, if you mean that naturalists will use that argument in their favor, then you are not wrong. I did not mean that. They will certainly do. They use anything they can in their favor.
But, if you mean that there is any sense in the idea that the derivation of new genes from non coding regions already existing in other species is in favor of naturalism, then you are wrong. That’s what I meant. So, it is up to you.
You ask:
“Common descent from what? Where did these coding sequences arise?”
Well, it is simple. If a non coding region is in the chimp, and a (presumably) functional ORF arises from it in humans, usually with only a few mutations, that mean two things:
1) The human ORF derives from the non coding sequence in chimps. That is best explained if descent of humans from chimps is true. Therefore, it is evidence if favor of common descent.
2) The non coding sequence in chimps already had most of the sequence information that will enable it to be functional once it becomes an ORF in humans.
Now, the simple point is that the non coding sequence in chimps (or any other precursor species) is not there from OOL. Whenever it originated, it originated by variation. And that variation is by definition “neutral”, because it does not affect any function.
Or, even if the non coding region were functional at other levels (for example, regulatory), and the variation that modifies it be negative, positive or neutral) that will be completely unrelated to the future ORF, which at present is not an ORF, is not translated and therefore is not visible to NS.
So, what we have is variation which is neutral, or anyway unrelated to the “ORF to come”, which builds in some way the correct sequence for the future functional protein, without any help from NS. Obviously, once the ORF is “completed”, and in some lucky way it becomes translated, then NS can help fixing it. But that mean nothing. The role of NS in a classical darwinist scenario is to build gradually the sequence, not just to use it when it is ready.
Now, the variation which builds the sequence before it becomes an ORF can only be:
a) Random
b) Designed
There are no other alternatives, except maybe the “algorithmic adaptation” scenario, which is even more in favor of design, but is not very plausible as a general mechanism of new gene formation.
Therefore, a naturalist who refutes design a priori is the very sad situation of believing that chance alone originated all the genes that originated that way, maybe most of the functional genes we know, if that is to be considered a general mechanism. That explanation makes no sense. I wish them good luck, because they will really need it.
PaV:
You ask:
“Question: It is being repeated here that a portion of non-coding DNA somehow becomes a ‘gene.’ How do we know that?”
In all the cases quoted here, we know that because of a strong homology between the new ORF (which is found only in the final species, for example in humans) and non coding sequences that are found in the precursor species (for example primates).
A strong homology is something that cannot be denies. It is a fact which cannot be explained as causal, and requires explanation. Simple derivation of the new sequence from the old one is the best explanation, IMO (obviously, that tells nothing of the mechanism of variation which produced the non coding region and which transforms it into the final ORF by a few last mutations). For that, as I have argued, designed engineering is the best, indeed the only explanation available.
In the paper we quoted about this scenario, such as this:
http://genome.cshlp.org/conten.....2.full.pdf
and this:
http://www.plosgenetics.org/ar.....02379-g002
(which was kindly provided by VJ on another thread)
the general idea is that the new genes are probably coding and functional. And there is some good evidence of their expression. And, if you look at figure 2 of the second paper, you will see that they are preferentially expressed in the brain and in the testes, which is exactly what we would expect of new functional genes which contribute to speciation.
I have not the references available now, but I think I remember a similar scenario is true on other species, probably drosophila, where new genes derived from non coding sequences have been found.
Pav:
Please, have a look at the 3 papers kindly provided by Evolve at post #49.
In the first (mouse gene) the gene is proved functional by a knockout experiment, and is expressed in the testis.
In the second one (drosophila) the abstract says:
“Comparative genomic analyses have revealed that genes may arise from ancestrally nongenic sequence. However, the origin and spread of these de novo genes within populations remain obscure. We identified 142 segregating and 106 fixed testis-expressed de novo genes in a population sample of Drosophila melanogaster. These genes appear to derive primarily from ancestral intergenic, unexpressed open reading frames, with natural selection playing a significant role in their spread. These results reveal a heretofore unappreciated dynamism of gene content.”
Emphasis mine. Please, note that NS is supposed to intervene only at the end, when the functional genes are already there.
The third link is again about further research in drosophila, but unfortunately it does not give any details (it is not a paper, but only a short news).
gpuccio you state:
So, correct me if I’m wrong, do you think God gradually transformed an ape into a human by some gradual ‘bottom up’ mechanism as Dr. Torley does??? If it is, that is a mighty large intellectual leap, hurdling over many empirical problems, you, and he, are making there!
I certainly don’t think you, or Dr. Torley, have such a firm foundation that you guys think that you do if you are making such a gargantuan leap to such a tentative conclusion for gradualness. For instance there is the little problem that you guys overlooked that genotypes (sequences) and phenotypes (body plans) do not map to one another,,
That is NOT a minor consideration!
Then there is the little problem that sequences can be highly similar in widely divergent species
Then there is the little problem of widely divergent genetic regulatory sequences,
Yet altering such regulatory sequences, involved in embryonic development, is found to be ‘always catastrophically bad’:
Yet, despite such a ‘catastrophically bad constraint’ for ‘bottom up’ mechanisms, and completely contrary to evolutionary thought, ‘new’ ORFan genes are found to be just as essential as ‘old’ genes in embryonic development:
Then there is the little problem that poly-functionality presents in terms of limiting any potential variability within a species’ body plan.
Then there is the little problem that multiple simultaneous ‘top down’ morphological alterations would be needed to accomplish such a transition:
I’m sure I’ve missed other criticisms that could be leveled, but I think the point is clear that the gradual ‘bottom up’ transition, envisioned by you, and Dr. Torley, is not nearly so easy as you might believe.
BA:
I don’t understand your problems.
I just commented that the recent evidence for the derivation of some genes from non coding genes is, if it is confirmed, a strong argument for design. I remain of this idea. In that case, the design would be gradual, guiding the transformation of the sequence until it is ready to be used in the right context.
I have never said:
a) That this is the only way new genes are designed. In other contexts, the realization of the new gene could be realized in shorter times, for example through guided transposon activity. However, all these theories can be evaluated according to facts, as we gather more understanding of molecular data. For example, a “quicker” appearance of new protein coding genes would give us orphan genes without any homology with non coding sequences in previous species.
b) That new orphan protein coding genes, however generated, can explain speciation. I absolutely agree with you that the most important part of new information in new species must be regulatory. Many times I have argued in that sense. That’s why the study of transcriptomes and of various RNA regulatory forms is of primary importance. I believe that we have at present very scarce understanding of the regulatory procedures, least of all of how they could “evolve”, or simply be generated.
c) If your problem is simply that you don’t accept common descent, that’s fine for me. I respect your opinion, but I am afraid that we have to disagree on that point, at least until I change my mind because of new facts, or of some different interpretation of known facts that convinces me (which is perfectly possible, but has not yet happened)
Finally, the ideas I have expressed here are mine and mine only. I am not sure what is VJ’s position on these issues, but he can certainly speak for himself.
BA:
Ah, you say:
“gradual ‘bottom up’ transition”. I don’t understand. The scenario I suggested is certainly “gradual”, but why “bottom up”?
A protein engineering through guided mutations, which is the only way a non coding sequence could be modeled to give a functional ORF, can be more or less gradual, but it is certainly “top down”, and not “bottom up”.
Could you please explain your point?
There just isn’t enough time for unguided evolution to produce a protein coding gene from non-coding DNA sequences. (see waiting for two mutations)
gpuccio, all I was pointing out is that your ‘sequential’ evidence for common descent is much weaker than you seem to realize. Here are a few more notes on the fact that ‘form’ is not reducible to sequential information as you seem to presuppose:
gpuccio, all I was pointing out is that your ‘sequential’ evidence for common descent is much weaker than you seem to realize. Here are a few more notes on the fact that ‘form’ is not reducible to sequential information as you seem to presuppose:
That comment from Dr. Walker reminds me of this comment from Dr. Hameroff:
Moreover,,,
,,,This preceding research also provides solid falsification for the late Rolf Landauer’s decades old contention that the information encoded in a computer is merely physical (merely ‘emergent’ from a material basis) since he believed it always required energy to erase it;
It is very interesting to note that quantum entanglement, which conclusively demonstrates that ‘information’ in its pure ‘quantum form’ is completely transcendent of any time and space constraints, should be found in molecular biology on such a massive scale, for how can the quantum entanglement ‘effect’ in biology possibly be explained by a material (matter/energy) ’cause’ when the quantum entanglement ‘effect’ falsified material particles as its own ‘causation’ in the first place? (J. Bell, A. Aspect. A. Zeilinger) Appealing to the probability of various configurations of material particles, as Darwinism does, simply will not help since a timeless/spaceless cause must be supplied which is beyond the capacity of the material particles themselves to supply! To give a coherent explanation for an effect that is shown to be completely independent of any time and space constraints one is forced to appeal to a cause that is itself not limited to time and space! i.e. Put more simply, you cannot explain a effect by a cause that has been falsified by the very same effect you are seeking to explain! Improbability arguments of various ‘special’ configurations of material particles, which have been a staple of the arguments against neo-Darwinism, simply do not apply since the cause is not within the material particles in the first place!
Stephen Meyer – Functional Proteins And Information For Body Plans – video
https://vimeo.com/91322260
Dr. Stephen Meyer comments at the end of the preceding video,,,
‘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. 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 – (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate – 2009)
Darwin’s Doubt narrated by Paul Giem – The Origin of Body Plans – video
http://www.youtube.com/watch?l.....page#t=290
BA:
Again, I don’t understand.
I said nothing about form and body plans.
I just said that homology is best explai ed by common descent.
The referenced article undermines Behe’s conclusions in the Edge of Evolution about 2 mutations. I have no idea of the mathematics used to justify this but they say they refute Behe. Now I don’t see just how much they refute him. Do they just reduce the time for these mutations to occur so the time required is still out of reach for anything meaningful to happen or do they reduce it to small amounts of time.
The condemnation is not as strong as one would expect if the second scenario took place.
They will say it does make sense. All naturalist believe the process is gradual but not all of them believe the only thing working is a natural selection of coding regions. Which is why I said that focusing all this attention on the neutral theory is a red herring.
There is a second process, they say that is also working very gradually, and it not subject to natural selection till at some time it gets transcribed into some meaningful piece of RNA which either produces a new protein or some RNA sequence that has function. Natural selection only affects coding regions that produce some transcribed sequence that then affects a survival characteristic of the organism. So for millions of years or more a DNA sequence is changing and is not subject to natural selection.
This ends up appearing to be a sudden event but actually will take millions of years. It is a long road to this functional sequence and and as I have just said during that time it was not subject to natural selection. The Brosius article was published in a tribute to Stephen Gould and it meant to establish why some aspects of evolution are sudden and others are not. He is giving a rationale for punctuated equilibrium.
I think it is futile to say the process does not exist when it obviously does. I also think it is futile to claim it is design when it is apparently the end result of some process that appears randomly. (this process may in fact be the result of a very intricately designed process to effect exactly what they say happens)
I believe the process that they describe will fall under its own weight because it is not robust enough to produce all the functional variation we see in biological species over the planet. So it here that the research should concentrate. Arbitrarily saying it is design or didn’t happen is not going to get ID anywhere. I believe the best approach is to say it is interesting but extremely inadequate. I proposed very testable hypotheses to look at this issue which I believe would bury not only the Darwinian version of evolution but this form of punctuated equilibrium.
I have not read any of the other recent comments so don’t know if I am just repeating what others have said.
“I said nothing about form and body plans.
I just said that (sequence) homology is best explai ed by common descent.”
Well if you say homology is best explained by common descent then it might be wise to considered if body plans might be reducible to sequence homologies. Just saying you are addressing the problem of ‘form’ from the wrong conceptual level!
“Humans and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart (38).
Associated with these anatomical differences there are, of course, major differences in posture (see cover picture), mode of locomotion, methods of procuring food, and means of communication. Because of these major differences in anatomy and way of life, biologists place the two species not just in separate genera but in separate families (39). So it appears that molecular and organismal methods of evaluating the chimpanzee human difference yield quite different conclusions (40).”
King and Wilson went on to suggest that the morphological and behavioral between humans and apes,, must be due to variations in their genomic regulatory systems.
David Berlinski – The Devil’s Delusion – Page 162&163
Evolution at Two Levels in Humans and Chimpanzees Mary-Claire King; A. C. Wilson – 1975
http://academic.reed.edu/biolo.....5(classic)
K´necting The Dots: Modeling Functional Integration In Biological Systems – June 11, 2010
Excerpt: “If an engineer modifies the length of the piston rods in an internal combustion engine, but does not modify the crankshaft accordingly, the engine won’t start. Similarly, processes of development are so tightly integrated temporally and spatially that one change early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream” (1)
http://www.uncommondescent.com.....l-systems/
jerry, Behe’s argument in “Edge” is that unguided evolution cannot produce two new protein folds. The two mutations in the article just referred to a binding site with what, 10 bases?
BTW Behe and the others did have a back-n-forth which is most likely on his UD site
The most interesting thing about the Meyer book was his emphasis in the latter part of the book on this non-genomic control of development. There may be a hunt for structure of the information for this as there was for DNA 60 years ago. And when they find it, the form may be so strange that it will be hard to interpret. When they found DNA they already had primitive digital codes to relate it to. Who knows what the structure will be that controls development and how it varies from species to species.
John Garvey has on his site a discussion about what makes human unique. It primarily references a paper by a population geneticist David Wilcox. Here is the Wilcox paper
http://www.asa3.org/ASA/meetin.....Wilcox.pdf
One of the things it says is that the regulatory nature in the human genome is extremely more complex than the next species. Here is a quote:
We are only a short way there to understanding what is happening. And all this appeared by chance?
Thank you. My comment at the end was then the correct assessment, that they really did not make much of a dent in Behe’s argument. It is typical that the naturalist when presented with the incredible improbability of what they espouse will resort to the trivial to defend their position.
In a very recent Teaching Company course on science, the lecturer resorts to the tree moths as an example to support Darwin. Either they are uninformed or just have no shame.
jerry, what if there is actual software that determines the final form? IOW even given all of the chemicals in a cell, including the membrane and cytoskeleton- just the hardware, nothing would happen without the controlling information that is none of the above.
To me THAT is the problem with biology. No one knows to look for such a thing because no one thinks it exists. Well except for a few of us.
It isn’t enough to arrange all of the parts of a computer in a the correct configuration. Without n OS and application programs it ain’t going to do much more than hold open doors and hold down papers.
But a lot of the so called junk DNA is extremely long sequences of repeating elements called LINES and SINES (Long Interspersed Elements and Short Interspersed Elements)
The biologist looking at this once said it obviously cannot code for anything, it is just repetitive nonsense and by implication proof of a non-designer. I believe there were Darwinist on this site who made this point. But if these sequences had no function, they would disappear over time because mutations would make them into non-repetitive nonsense fairly quickly.
But the fact that they are conserved means they are subject to natural selection which is preventing these regions from mutating. It must mean they have an important function and it appears that regulation is it.
Meyer talks about the sugar codes in his book. They will look for it big time when it becomes obvious that it is controlling major events in development. Some may be doing that already. Maybe it will be digital in form, maybe not and if that is so then it may lead programmers to a new type of computing programming approach, one that is not digital.
BA at #90:
I don’t want to be fastidious, but I want to clarify well my position.
You say:
So, I can only state again thyat I am not addressing the problem of “form” at all!
I say that homology is best explained by common descent. That means exactly what it means, and nothing else. Can you find any reference to the problem of form or body plans in that statement?
IOWs, what I say is:
If a (a non coding sequence) in species A presents strong homology to b, an ORF in species B, common descent is the best explanation. That only means that the sequence b in B derives from the pre-existing sequence a in A, through some form of physical continuity.
Obviously, it is the designer who modifies the sequence a so that it becomes b. Similarly, it is the designer who prepares the sequence a, so that in a second time it may become b. Nothing of that happens by chance. It is top down design all the way.
Am I saying that the homology between a and b explains the new form or body plan in B? No, not at all. We simply don’t know what determines a new form or body plan. I am sure that whatever it is, it will be shown to be the product of design, but I must say that IMO at present we don’t know for sure how a body form or body plan is controlled. So, I am not affirming anything about what generates the new body plan. It could be a gradual process, or something more similar to a miracle. I just don’t know.
When I say that I accept common descent, I mean something very simple: whatever is the process that generates a new species, that process works, at least in some measure, on the species that already exists. And the reasons why I think so are many, and all of them are at the molecular level. The facts in favor of a derivation of new genes from existing non coding genes are among them.
I am well aware that not all molecular observations are in favor of CD, and that some of them cast serious doubts on the idea of an universal CD. I am very interested in all the facts that will be discovered that can bring new light to the issue.
But, for the moment, I remain of the idea that CD is the best explanation. And I state, again, that this implies nothing about the origin of new forms and body plans.
I hope that is clear.
gpuccio, if you have no viable connection between sequences and body form, the argument for common descent of body forms from sequence homologies (tenuous as the sequence comparisons are as you yourself admit) collapses.
Long repetitive sequences (LINEs and SINEs) clearly do not have a coding function, as they lack promoter sequences (which are absolutely necessary for a sequence to be transcribed and subsequently translated). However, they may have other biological functions. For example, the coding sequences in eukaryotic DNA are not entirely randomly located. Rather, they are located in parts of the genome that allow them to be associated with the histone proteins in nucleosomes. This is because modification of DNA binding to histones is an important mechanism of gene regulation in eukaryotes. Therefore, the “spacer” non-coding DNA such as LINEs and SINEs could still influence the expression of genes located at significant distances away by modifying their binding to histones in nucleosomes.
As for the “engines of variation,” I would like to emphasize that the kind of variation I have written about is both genetic and phenotypic variation. Indeed, the majority of the mechanisms I listed in my “engines of variation” posts at The Evolution List are mechanisms that primarily affect gene expression, rather than gene sequence. Regulation of gene expression in eukaryotes is both complex and massive (I know, I’m teaching a course in it right now). Simply knowing the number of coding sequences in the genome of a multicellular eukaryote (especially an animal), for example by knowing the number and location of promoter sequences, tells you almost nothing about how the coding sequences (i.e. “genes”) are expressed and regulated. There are hierarchical biochemical systems involving anti-sense RNAs, small polypeptides, proteins, and non-coding sequences in DNA that all interact to produce the components of the phenotype. Increasingly fine-grained analyses of these systems has revealed that many of them are “kludges;” that is, they work, but not well and not always consistently. This “kludginess” of gene expression/regulation in eukaryotic cells is an apparently inescapable concomitant of both the complexity of the systems involved and the history of their implementation Think about how kludgy a huge OS like Windows has become; it’s essentially a small core of original integrated code, massively modified by an almost uncountable patchwork of “bug fixes” and “extensions.” The surprising thing about such systems is not that they don’t work well (they don’t), but rather that they work at all.
It is becoming clear that the “software” of a typical eukaryotic cell is really mostly “kludgeware.” It generally works “just good enough” to not self-destruct. And, as it is replicated and modified (and especially as “foreign” sequences are introduced into it or removed from it by retrotranspositions, transposons, retroviral insertions, polymerase “skip-copying” and other “noise” events), it stumbles along in much the way that “Mendel’s Accountant” and the nearly-neutral theories predict that it should.
This is one of the main reason that germ cells are set aside very early in embryonic development in eukaryotes. The less often the genome is replicated, the fewer mistakes it accumulates. This is part of what is wrong with “Mendel’s Accountant:” it doesn’t take into account the particular kinds of cells that actually constitute the ongoing phylogenetic lines it purports to describe. THe MA model assumes that all cells change randomly at approximately constant rates, yet germ cells don’t change at anything like the same rates as most cells, primarily because they don’t undergo mitotic divisions at anything like the rates of most other cells.
And may I say that gpuccio is entirely correct about the idea that homologies (combined with shared derived sequences) are indeed very strong evidence for common descent. This is especially the case for non-coding sequences that have little or no effect on phenotypes. There are a multitude of examples of homologous sequences that either have no effect on phenotypes or have surprisingly different effects in different organisms as a result of modified gene expression in diverging phylogenetic lines. The assertion that the origin of such homologies is the result of the intervention of an intelligent designer, however, is not empirically verifiable or falsifiable, and so I won’t address it.
As for how functional orphans can arise from non-coding sequences, one first has to specify what kind of non-coding sequences one is referring to. If one means LINEs and SINEs, then I agree completely. Transforming a very long sequences of repeated tandem repeats into a coding sequence, complete with a promoter, terminator, and enhancing sequences would indeed be miraculous. However, a significant fraction of the non-coding sequences in eukaryotes consist of sequences that were once viable coding sequences. These either were corrupted and thereby inactivated by mis-replication of their promoters/enhancers or (more commonly) were inserted into the genome as the result of retrotransposition, reverse transcription, transposon insertion, and similar processes, in which coding sequences with functional promoters, terminators, and enhancers are inserted or removed from the genome. In a great many cases, such sequences are quickly identified and inactivated by “surveillance/editing” mechanisms, which identify and inactivate the “rogue” sequences by inactivating their promoters and/or enhancers.
However, this means that “dead” former coding sequences are scattered throughout the genome and can be reactivated by inserting new, active promoters/enhancers that can reactivate part or all of the “dead” sequences. This has actually been accomplished in the laboratory, where a “dead” retroviral sequence estimated at being inactive for millions of generations was “resurrected” by providing it with an active promoter sequence. The “fossil” sequence then acted like a functional virus, infecting host cells and generally acting like “its old (now extinct) self.”
So, can reactivation of non-coding sequences produce new, functional gene sequences? Yes, if the non-coding sequences were once active coding sequences that had been inactivated by modification of their promoters/enhancers.
BTW, my thanks to Jerry for alerting me to this thread and the questions directed to me.
Mr MacNeill you claim:
Unfortunately for you and your Darwinian thought police buddies, you do not get to decide what constitutes strong empirical evidence and what does not. Especially for the tea leaf reading enterprise of Darwinian evolution. The FACT the there is no empirical correlation between sequences and body plan morphogenesis, as well as the FACT that sequences, especially regulatory, are ‘all over the place’, pretty much makes the argument for correlation to collapse. ‘Just so stories’ do not help your pseudo-scientific Darwinian fantasies.
Darwinism is a Pseudo-Science – Part II
What the vast majority of Darwinists fail to realize (or ever honestly admit to) is that Darwinian evolution is not even a ‘real’ physical science in any proper sense 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, admits that Darwinian evolution lacks the rigor of a proper physical science:
The main reason why Darwinian evolution is more properly thought of as a pseudo-science instead of a proper science is because Darwinian evolution has no rigid mathematical basis, like other overarching physical theories of science do. A rigid mathematical basis in order to potentially falsify it (in fact math, in so far as math can be applied to Darwinian claims, constantly shows us the Darwinian evolution is astronomically unlikely),,
Another primary reason why Darwinian evolution is more realistically thought of as a pseudo-science rather than a proper physical science is that Darwinian evolution does not have a demonstrated empirical basis to support its claims (in fact empirical evidence also consistently shows us that Darwinian evolution is astronomically unlikely),,
Another reason why Darwinian evolution is more realistically thought of as a pseudo-science rather than a proper physical science is that the two foundational pillars of Darwinian evolution, Random Mutation/Variation and Natural Selection, are both now shown to be severely compromised as to having the causal adequacy that Darwinists have presupposed for them. For instance, although Darwinian evolution appeals to unguided ‘random mutations/variations’ to DNA as the main creative source for all evolutionary novelty, there are now known to be extensive layers of error correction in the cell to protect against any unguided “random” changes happening to DNA in the first place:
Moreover, for the vast majority of times that changes do happen to DNA, they are now known to be ‘directed changes’ by sophisticated molecular machines, not unguided ‘random changes’ from a cosmic ray, chemical imbalance, or some such entropy driven event as that:
What should be needless to say, having ‘cell-mediated processes’ direct changes to DNA is in direct contradiction to the ‘undirected randomness’ which is held to be foundational to neo-Darwinian thought.
Moreover, Natural Selection, that other great pillar upon which Darwinian evolution rests, has also been undermined as having the causal adequacy that neo-Darwinists have attributed to it. First off, to the extent that Natural Selection does do anything, Natural Selection is found to be a eliminative force not a generative force:
As well, Natural Selection is grossly inadequate to do the work required of it because of what is termed ‘the princess and the pea’ paradox. The devastating ‘princess and the pea’ paradox is clearly elucidated by Dr. John Sanford, at the 8:14 minute mark, of this following video,,,
Dr. Sanford points out, in the preceding video, that Natural Selection acts at the coarse level of the entire organism (phenotype) and yet the vast majority of mutations have effects that are only ‘slightly detrimental’, and have no noticeable effect on phenotypes, and are thus far below the power of Natural Selection to remove from genomes before they spread throughout the population.
Here are a few more notes on this insurmountable ‘princess and the pea’ problem for natural selection:
Moreover, as if that were not devastating enough as to undermining any credibility Natural Selection might have had as to having the causal adequacy to explain the highly integrated levels of overlapping functional information found in organisms, dimensionally speaking, Natural Selection is now known to not even be on the right playing field in the first place:
Here is, what a Darwinist termed, a ‘horrendously complex’ metabolic pathway (which operates as if it were ’4-Dimensional):
And remember, Darwinian evolution has yet to explain a single gene of those ‘horrendously complex’ metabolic pathways.
The reason why a ‘higher dimensional’ 4-Dimensional structure, such as a ‘horrendously complex metabolic pathway, would be, for all intents and purposes, completely invisible to a 3-Dimensional process, such as Natural Selection, is best illustrated by ‘flatland’:
I hold that the reason why internal physiology and anatomy operate as if they were four-dimensional instead of three dimensional is because of exactly what Darwinian evolution has consistently failed to explain the origination of. i.e. functional information. ‘Higher dimensional’ information, which is bursting at the seams in life, simply cannot be reduced to any 3-dimensional energy-matter basis:
Moreover, matter and energy are now both shown to reduce to ‘quantum information/entanglement’. In fact an entire human can now, theoretically, be reduced to quantum information and teleported to another location in the universe:
Thus not only is Information not reducible to a 3-Dimensional energy-matter basis, as is presupposed in Darwinism, but in actuality energy and matter both reduce to a information basis as is presupposed in Christian Theism:
Why the Quantum? It from Bit? A Participatory Universe?
Excerpt: In conclusion, it may very well be said that information is the irreducible kernel from which everything else flows. Thence the question why nature appears quantized is simply a consequence of the fact that information itself is quantized by necessity. It might even be fair to observe that the concept that information is fundamental is very old knowledge of humanity, witness for example the beginning of gospel according to John: “In the beginning was the Word.”
Anton Zeilinger – a leading expert in quantum teleportation:
Verse and Music:
John 1:1-4
In the beginning was the Word, and the Word was with God, and the Word was God. He was in the beginning with God. All things were made through Him, and without Him nothing was made that was made. In Him was life, and the life was the light of men.
Redeemed – Big Daddy Weave
http://myktis.com/songs/redeemed/
Look, BA, evolutionary biology provides the most likely explanation for our existence as a species as far as science is concerned. Your buddies here can ignore science all they want, but the fact remains that evolution is the best that we can come up with based on reason. Your “intelligent design” hypothesis is interesting, but leads to nowhere, as there is no evidence to back it up.
Enjoy convincing the scientific illiterate otherwise.
BA:
This is becoming a little bit embarassing. I never made an “argument for common descent of body forms from sequence homologies”. I just made an argument for common descent. I still don’t understand where body forms are mentioned or implied in my argument. Please, explain, or just let it be.
Don’t bother. “Because science can’t explain exactly how organisms develop, that means that science is wrong.” Welcome to the world of UD.
So body forms don’t matter in your argument for common descent? Only sequence homologies matter in your argument for common descent?
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/
now THAT’S embarrassing!
How is that embarrassing? Obviously all life that is based on the same properties is going to have similar structures an functions. Care to elaborate on this, or are you just quote mining?
Allen_MacNeill:
Thank you for your very interesting contribution.
Just a few comments.
1) I am absolutely convinced that non coding DNA, including
long repetitive sequences, can have a lot of functions. Some of them we already understand, and many we will probably understand better in the future. If you look at my post #76, you will see that I wrote there:
“Now, the simple point is that the non coding sequence in chimps (or any other precursor species) is not there from OOL. Whenever it originated, it originated by variation. And that variation is by definition “neutral”, because it does not affect any function.
Or, even if the non coding region were functional at other levels (for example, regulatory), and the variation that modifies it be negative, positive or neutral) that will be completely unrelated to the future ORF, which at present is not an ORF, is not translated and therefore is not visible to NS.
So, what we have is variation which is neutral, or anyway unrelated to the “ORF to come”, which builds in some way the correct sequence for the future functional protein, without any help from NS. Obviously, once the ORF is “completed”, and in some lucky way it becomes translated, then NS can help fixing it. But that mean nothing. The role of NS in a classical darwinist scenario is to build gradually the sequence, not just to use it when it is ready.”
(Emphasis added).
So, my point is very simple: even if non coding sequences are functional, that function is obviously non related to their sequence as a potential symbolic sequence that codes for AAs. Therefore, even if NS acts on RV of the non coding sequence, it will act in a way that is completely random in relation to the “coding sequence to come”. Therefore, the “evolution” of he future ORF remains completely random in this scenario.
2)You say:
That’s exactly what makes your list wholly ambiguous.
I will try to be more clear.
The “mechanisms that primarily affect gene expression” are a bulk of information that is transmitted, and indeed efficiently transmitted, if species continue to exists in time. Therefore, that information must be in the genome, or in some epigenetic configuration. Wherever it is, it is functional information, and it is part of the “genome” in a wide sense (the total information that is transmitted from being to being in reproduction).
Therefore, that regulatory information is part of the “genotype” (in a wide sense), and is not a “phenotype”. Any variation acquired by interaction with the environment will not be part of that wide “genotype” unless and until it is integrated in some way in what is transmitted.
I have nothing against neo Lamarkism: it certainly is an important part of our new understanding of molecular mechanisms. But, again, if and when neo Lamarkian mechanisms are proved to exists, they will be adaptive mechanisms, which willl show high organization and functional information in the mechanisms itself.
I have cited many times the mechanism of somatic antibody maturation as a very good example of the genetic engineering of existing genes in response to environmental information (the contact with specific epitopes). Even if that mechanism does not generate transmittable information (because it takes place in somatic cells), it is a good example of an adaptive mechanism. But it is extremely complex and functional, and is in itself a very good argument for design of the mechanism itself.
That’s why your list is ambiguous. It does not discriminate between the mechanisms which are only “variations of random variation” and those which, if proved, would be complex functional adaptation which incorporate environmental information into transmittable information. And it does not discriminate between true explanatory mechanisms and simple vague suggestions of possible results of unknown mechanisms.
IOWs, it is not useful to just mention a lot of supposed “engines of variation” without detailing why they are engines, and what type of variation they can explain.
3) You say:
I agree. And so?
Protein coding genes are the final effectors. Regulatory information is obviously the real thing. And so?
Regulatory information is as much a part of the genotype (be it in the narrow sense, that is written in DNA configurations, or in the wider sense which includes epigenetically transmitted information) as protein coding genes.
Where do you think that “anti-sense RNAs, small polypeptides, proteins, and non-coding sequences in DNA” are written and transmitted? They certainly “interact to produce the components of the phenotype”, but they are transmitted information.
In my arguments for a design inference for biological information, I stick to protein coding genes for a very simple reason: they are what we know better. We know the code, we know how they work, so it’s easier to make a detailed and quantitative argument for them.
But there is no doubt that regulatory information is a level of higher functional information, and it is a potentially much stronger evidence for design.
4)About your “kludgeware” argument.
I will not debate whether the biological designer can really be compared to Microsoft designers :). One of the two could take offense!
But I will make a very simple point: good or bad, designers they are all the same.
However, I certainly agree with a very important point, which I have made myself many times. You say:
That’s perfectly true.
The more a system is complex, the more it is “frail”, the more it needs complex functional subsystems to allow its bare survival: complex error management systems, and so on. That is always true, however good or bad the implementation of the system is, and especially, as you correctly mention, if ad when the implementation of the system is sequential (which I absolutely believe, as you will have understood from my defending Common Descent here).
This is, in itself, one of the most powerful arguments against any kind of darwinian evolution, based on the concepts survival and reproductive advantages, and ID theory, based on the concept of functions and the need to implement new, ever more complex, functions as the “driving engine” of designed evolution.
The simple fact is: optimal survival and reproduction were already achieved at the beginning of OOL, with prokaryotes. Prokaryotes are still the most successful, and simplest, biological reproducing beings. All the complexity which has been added has made new beings, up to humans, more frail, less efficient in survival and reproduction, much more dependent on very complex repair and defense mechanisms. IOWs, much more strictly design dependent.
5) You say:
That is simply not true. ID is all about the empirical verification of the origin of functional information from an intelligent designer. All the arguments I have ever made here are exclusively about that. Empirical design inference. You may not agree that ID is in any way successful in its empirical purpose, but simply dismissing it by saying that “is not empirically verifiable or falsifiable, and so I won’t address it” is really pointless.
Many times I have shown here that the fundamental statements of ID (about complex functional information in biological molecules, and the design inference from it) are completely ans simply falsifiable, and therefore perfectly scientific.
6) Finally, about “functional orphans”. I find your final argument really strange. If I understand you well, you are simply suggesting that new functional orphan genes are simply the reactivation of inactivated older genes.
But that would simply mean that their functional information is old. First of all, it would not explain in any way how that information was generated in the beginning. New orphan genes would simply be old genes which are recruited again.
But, beyond the complete lack of explanatory power of such a scenario, it is however wholly implausible. In some of the papers we quoted here, extensive checks have been made to exclude that the new orphans were some kind of recently inactivated genes. And obviously, they have no homologies with any known protein coding genes in the whole known proteome. That’s exactly why they are called “orphans”.
So, I am very happy that you state that:
Because that’s exactly what we observe, and probably will observe ever more as our knowledge and understanding increases.
Thank you for the info Allen. Nice to hear from you.
What textbook are you using to teach these topics?
BA:
Yes. I hope that is clear now.
Not at all! It’s simply interesting.
As I already said (but you seem not to consider what I write):
“I am well aware that not all molecular observations are in favor of CD, and that some of them cast serious doubts on the idea of an universal CD. I am very interested in all the facts that will be discovered that can bring new light to the issue.
But, for the moment, I remain of the idea that CD is the best explanation. And I state, again, that this implies nothing about the origin of new forms and body plans.”
Emphasis added.
Well, that remains my position. And I have no reason to be embarrassed by it.
AVS:
Long time, no see! Please, stay. We really need you to lift our mood. 🙂
AVS:
Yet evolutionary biology can’t explain anything as unguided evolution cannot be modelled nor tested. It doesn’t produce any predictions and is useless as a research heuristic.
And yet AVS can’t say what science we are ignoring- quite the lying coward this one is
And yet we have provided the evidence to back it up and said where it leads.
AVS- ignorant and proud of it.
AS for Allen’s “engines of variation”, it should be noted that no one has any methodology to determine that they are blind and undirected processes. On the contrary we know that regulation requires guidance. Something has to know what to regulate, when to regulate and how much to regulate.
The same goes for transcription, editing, proof-reading and error-correction.
Only evolutionary propaganda sez these are blind and undirected processes- just because we can observe them happening without any observed intervention! And that is beyond pathetic.
“sez”?
Joe, you’re definitely a pre-pubescent with a single-digit IQ. No wonder you fit in here at UD.
AVS you are definitely a cowardly projector. You trying to insult me is laughable. But I understand that is all you have.
BTW sez fits because you definitely cannot support anything you post wrt biology and evolution. You are nothing but a deluded little punk first year biology student.
gpuccio, though I usually greatly respect your opinion (and your work in general against Darwinists), your reason for supporting common descent lacks much to be desired empirically. If body forms are disregarded and sequences are allowed priority, as you hold, even though there is severe incongruousness in sequence data, and even though information of ‘form’ is not reducible to sequential information, then how is your view to be regarded with any more respect than the typical Darwinian views? i.e. regarded as empirically relevant and ‘scientific’? You are basically stating your personal opinion as if it should have ‘scientific’ weight, and, as far as empirical evidence is concerned, there is not such weight to be had for your opinion.
a few notes to that effect:
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
podcast – Molecular Data Wreak Havoc on (Darwin’s) Tree of Life – Casey Luskin – March 2014
http://intelligentdesign.podom.....7_31-07_00
Shark Proteins Contradict the Standard Phylogeny of Vertebrates – Casey Luskin – January 6, 2014
Excerpt: there’s almost no dataset that can contradict (falsify) common descent. Every time you find that one trait predicts one phylogeny, and another trait predicts a conflicting phylogeny, you can effect a reconciliation by invoking at will more evolutionary steps of convergent loss or gain of traits, or invoking a host of other ad hoc explanations. In a worst case scenario, if genes were distributed in the most un-treelike manner imaginable, I suppose you could take all the known genes present in the most recent presumed common ancestor of that group, and then simply invoke losses (and gains) of genes to reconcile the observed distribution with a tree. –
http://www.evolutionnews.org/2.....80781.html
BA:
Just to know, how do you explain the following two observations?
1) Homologies between non coding sequences and new orphan genes (as discussed here).
2) Sequence differences in structurally and functionally similar homologous proteins in species, with differences usually increasing in more distant species.
With that, I have no personal agenda about CD. I have no reason to accept it and no reason to reject it, out of what I sincerely think because of the facts I know. I have absolutely no religious or philosophical position about common descent.
Moreover, I don’t think that at present we have a definite tree of life which is consistent or credible. I am aware that trees of life generate great inconsistencies according to how they are built. Maybe that means that no tree of life exists, and that CD needs to be reconsidered. Or maybe it means something about the validity, or lack of it, of the different methods used. Or maybe it means something else, that we still need to understand. Whatever it is, I am very interested in understanding it.
I don’t believe that CD should necessarily be universal, nor that it must be the only or even the main modality of evolution. I am fully open to any interpretation, provided that facts and good scientific reasoning be in favor of it.
I thank you sincerely for your respect, and I want to ensure you that I appreciate very much your contributions here. You have given me many fundamental ideas and informations. And I believe we share the most fundamental ideas about design in biology.
So, I fully respect your position. Please, do the same with mine.
as to:
1) Homologies between non coding sequences and new orphan genes (as discussed here).
Orphan Genes (And the peer reviewed ‘non-answer’ from Darwinists) – lifepsy video
http://www.youtube.com/watch?v=1Zz6vio_LhY
and
2) Sequence differences in structurally and functionally similar homologous proteins in species, with differences usually increasing in more distant species.
(FoxP2) Dawkins Best Evidence Refuted – video
https://www.youtube.com/watch?v=IfFZ8lCn5uU
BA:
Is it possible to have your personal answers and arguments? I don’t like to discuss with videos.
Via the videos, I don’t find your points empirically strong to the conclusion you would like to make. Via the sheer disconnect between information for form and information for sequences (Meyer) I don’t find your beliefs to be scientifically relevant. Via the punctuated fossil record (Gould) I don’t find your beliefs to be anything more than philosophical presuppositions. i.e. the case for common descent simply is not there empirically.
BA:
OK, thank you. I don’t really understand your points, but that’s fine.
http://www.icr.org/article/9145
Genetic Gap Widens Between Humans and Chimps
by Jeffrey P. Tomkins, Ph.D. *
Evidence for Creation › Evidence from Science › Evidence from the Life Sciences › All Life Systems Were Created by God › DNA Was Created as a Reservoir for the Information of Life
Increasingly, orphan genes defy evolution and support the Genesis account of creation. These genes are unique sets of coding sequences specific to particular creatures. This is a big problem for evolutionary ideas to explain. In a recent research report, scientists describe a new set of 1,307 orphan genes that are completely different between humans and chimpanzees.1
Orphan genes, as the name implies, are found in no other type of creature and therefore have no evolutionary history. This finding is another key prediction of the creation model. Not only should creatures have similar code for similar functions, but they should also have unique code that makes them distinct from other creatures. In support of this creation prediction, scientists discovered that orphan genes are incredibly important for specific biological processes and traits that correspond with specialized adaptations. Several previous articles published on the ICR news site have described these types of genes discovered in zebrafish and honey bees.2,3
Many creatures with similar types of body plans and other shared biological traits, possess similar sets of core genes. Evolutionists claim that this is evidence of common ancestry. However, creationists propose a more obvious and efficient explanation: Common genetic code is a predicted feature of purposefully engineered systems in the genomes of creatures that share the same environment and have similar requirements. It’s just like a computer programmer who uses common pieces of code in different software programs.
In yet another recent research report, scientists describe 634 orphan genes in humans and 780 in chimpanzees.1 In other words, we now have a new set of 1,307 genes that are completely different between humans and chimpanzees. In fact, the chimp-specific genes are not found in any other supposed chimp ancestor—like macaque, an extant monkey. They are unique to the chimps just like the human orphan genes are unique to humans. Darwinian evolution did not predict this remarkable discovery.
Essentially exposing evolution’s weakness in explaining orphan genes, the researchers say, “For the past 20 years scientists have puzzled over a strange-yet-ubiquitous genomic phenomenon; in every genome there are sets of genes which are unique to that particular species i.e. lacking homologues [similar counterparts] in any other species.”1
Another interesting fact about these newly discovered orphan genes is that they represent just a subset of the genes unique to chimp or human. The researchers only analyzed genes expressed in liver, heart, brain, and testes. Many other bodily tissues still need to be examined. In addition, the team only analyzed genes that were spliced, meaning complex genes that have coding and non-coding regions, with the coding regions being snipped out of the RNA transcript after they are copied from the DNA. Many other genes in the genome are not spliced and were not included in this study. Needless to say, the numerous gene differences that scientists discovered between humans and chimps cannot be accounted for by Darwin’s theory of common ancestry.
Not only do orphan genes and the amazing creature-specific traits they encode challenge evolution, they also help creationists understand the patterns of genome structure related to created kinds. While obvious differences between humans and chimps defy evolution on a grand scale, the presence of orphan genes underscores the uniqueness of humans created in God’s image.
BA77, I have put up the Dawkins video clip and some screen shots on the FOXP family: http://www.uncommondescent.com.....mily-tree/ Let us see what this is, gross error by Dawkins or the grand daddy of all hoaxes and quote mines. KF
tjguy @126,
Excellent point.
That we find in a genome both code-reuse and code specific to the given kind is precisely what intelligent design predicts. It is exactly what programmers do all day long: Reuse code where possible and add new code specific to whatever new features an application requires.
What is more difficult is to write software that will run on various operating systems and hardware, and will cope with unexpected, undefined input and still function meaningfully. For the software of life, “functioning meaningfully” is surviving long enough to reproduce. This requires an adaptability being built into life’s software that is way beyond human-written software.
We already knew from experience with “artificial” selection, like dog breeding, that a given kind could have a wild variety of possible traits. Dog breeders had powerfully demonstrated this, and if evolution worked the way Darwin had proposed, breeders would have eventually bred dogs into something that couldn’t be called a dog. That didn’t happen.*
So, what the canine genome contained was the information to construct a wild variety of canines, but nothing else; it appears to be information composed for a specific purpose: the creation of a particular kind. The adaptability to changing environments provided by the various versions of dogs that can be derived from that information indicates its composer’s genius as well His intentions: The dog-kind was to last for a while. The fossil record is full of evidence that a given kind suddenly appears and lasts until the magnitude of the changes to the environment exceeds the adaptability of that kind. It’s as though it was all preprogrammed. Maybe that’s because it was. ;o)
* Yes, I know the objection: “Dog breeders haven’t been at it for millions of years.” That objection fails miserably. What would take forever to happen mindlessly and accidentally, like the scattered jigsaw puzzle pieces of a 500 piece puzzle being correctly assembled accidentally, takes only a few hours for an intelligence to accomplish. If evolution worked the way Darwin proposed, dog breeders would have bred dogs into something else by now. We now know that didn’t happen because the information required to build something else just isn’t in the “dog-kind” genome. That information is as unlikely to be arrived at accidentally as it is for that jigsaw puzzle to get assembled accidentally, which is to say that it just isn’t going to happen.