Intelligent Design

So, why are the human and chimpanzee/bonobo genomes so similar? A reply to Professor Larry Moran

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Professor Larry Moran has kindly responded to my recent post questioning whether he, or anyone else, understands macroevolution. In the course of his response, titled, What do Intelligent Design Creationists really think about macroevolution?, Professor Moran posed a rhetorical question:

I recently wrote up a little description of the differences between the human and chimpanzee/bonobo genomes showing that those differences are perfectly consistent with everything we know about mutation rates and the fixation of alleles in populations [Why are the human and chimpanzee/bonobo genomes so similar?]. In other words, I answered Vincent Torley’s question [about whether there was enough time for macroevolution to have occurred – VJT].

That post was met with deafening silence from the IDiots. I wonder why?

I’ve taken the trouble to read Professor Moran’s post on the genetic similarity between humans, chimpanzees and bonobos, and I’d like to make the following points in response.

1. Personally, I accept the common ancestry of humans, chimpanzees and bonobos. Of course, I am well aware that many Intelligent Design theorists don’t accept common ancestry, but some prominent ID advocates do. Why do I accept common descent? Because I think it’s the best explanation for the pattern of similarities we find between humans, chimpanzees and bonobos. Young-earth creationist Todd Wood (who is also a geneticist) has freely acknowledged that it is difficult to explain these similarities without assuming common ancestry, in his 2006 article, The Chimpanzee Genome and the Problem of Biological Similarity (Occasional Papers of the BSG, No. 7, 20 February 2006, pp. 1-18). Referring to studies which highlight these similarities, he writes:

Creationists have responded to these studies in a variety of ways. A very popular argument is that similarity does not necessarily indicate common ancestry but could also imply common design (e.g. Batten 1996; Thompson and Harrub 2005; DeWitt 2005). While this is true, the mere fact of similarity is only a small part of the evolutionary argument. Far more important than the mere occurrence of similarity is the kind of similarity observed. Similarity is not random. Rather, it forms a detectable pattern with some groups of species more similar than others. As an example consider a 200,000 nucleotide region from human chromosome 1 (Figure 2). When compared to the chimpanzee, the two species differ by as little as 1-2%, but when compared to the mouse, the differences are much greater. Comparison to chicken reveals even greater differences. This is exactly the expected pattern of similarity that would result if humans and chimpanzees shared a recent common ancestor and mice and chickens were more distantly related. The question is not how similarity arose but why this particular pattern of similarity arose. To say that God could have created the pattern is merely ad hoc. The specific similarity we observe between humans and chimpanzees is not therefore evidence merely of their common ancestry but of their close relationship.

Evolutionary biologists also appeal to specific similarities that would be predicted by evolutionary descent. Max’s (1986) argument for shared errors in the human and chimpanzee genome example of a specific similarity expected if evolution were true. This argument could be significantly amplified from recent findings of genomic studies. For example, Gilad et al. (2003) surveyed 50 olfactory receptor genes in humans and apes. They found that the open reading frame of 33 of the human genes were interrupted by nonsense codons or deletions, rendering them pseudogenes. Sixteen of these human pseudogenes were also pseudogenes in chimpanzee, and they all shared the exact same substitution or deletion as the human sequence. Eleven of the human pseudogenes were shared by chimpanzee, gorilla, and human and had the exact same substitution or deletion. While common design could be a reasonable first step
to explain similarity of functional genes, it is difficult to explain why pseudogenes with the exact same substitutions or deletions would be shared between species that did not share a common ancestor.

Nevertheless, Wood feels compelled to reject common ancestry, since he believes the Bible clearly teaches the special creation of human beings (Genesis 1:26-27; 2:7, 21-22). Personally, I’d say that depends on how you define “special creation.” Does the intelligent engineering of a pre-existing life-form into a human being count as “creation”? In my book it certainly does.

2. In his post, Professor Moran (acting as devil’s advocate) proposes the intelligent design hypothesis that “the intelligent designer created a model primate and then tweaked it a little bit to give chimps, humans, orangutans, etc.” However, he argues that this hypothesis fails to explain “the fact that humans are more similar to chimps/bonobos than to gorillas and all three are about the same genetic distance from orangutans.” On the contrary, I think it’s very easy to explain that fact: all one needs to posit is three successive acts of tweaking, over the course of geological time: a first act, which led to the divergence of African great apes from orangutans; a second act, which caused the African great apes to split into two lineages (the line leading to gorillas and the line leading to humans, chimps and bonobos); and finally, a third act, which led humans to split off from the ancestors of chimps and bonobos.

“Why would a Designer do it that way?” you ask. “Why not just make a human being in a single step?” The short answer is that the Designer wasn’t just making human beings, but the entire panoply of life-forms on Earth, including all of the great apes. Successive tweakings would have meant less work on the Designer’s part, whereas a single tweaking causing a simultaneous radiation of orangutans, gorillas, chimps, bonobos and humans from a common ancestor would have necessitated considerable duplication of effort (e.g. inducing identical mutations in different lineages of African great apes), which would have been uneconomical. If we suppose that the Designer operates according to a “minimum effort” principle, then successive tweakings would have been the way to go.

3. But Professor Moran has another ace up his sleeve, for he argues that the number of mutations that have occurred since humans and chimps diverged matches the mutation rate that has occurred over the last few million years. In other words, time is all that is required to generate the differences we observe between human beings and chimpanzees, without any need for an Intelligent Designer:

The average generation time of chimps and humans is 27.5 years. Thus, there have been 185,200 generations since they last shared a common ancestor if the time of divergence is accurate. (It’s based on the fossil record.) This corresponds to a substitution rate (fixation) of 121 mutations per generation and that’s very close to the mutation rate as predicted by evolutionary theory.

Now, I suppose that this could be just an amazing coincidence. Maybe it’s a fluke that the intelligent designer introduced just the right number of changes to make it look like evolution was responsible. Or maybe the IDiots have a good explanation that they haven’t revealed?

Some mathematical objections to Professor Moran’s argument

Professor Moran makes the remarkable claim that 130 mutations are fixed in the human population, in each generation. Here are a few reasons why I’m doubtful, even after reading his posts on the subject (see here, here and here):

(a) most mutations will be lost due to drift, so a mutation will have to appear many times before it gets fixed in the population;
(b) necessarily, the mutation rate will always be much greater than the fixation rate;
(c) nearly neutral mutations cannot be fixed except by a bottleneck.

I owe the above points to a skeptical biologist who kindly offered me some advice about fixation. As I’m not a scientist, I shall pursue the matter no further. Instead, I’d like to invite other readers to weigh in. Is Professor Moran’s figure credible?

Professor Moran is also assuming that chimps and humans diverged a little over five million years ago. He might like to read the online articles, What is the human mutation rate? (November 4, 2010) and A longer timescale for human evolution (August 10, 2012), by paleoanthropologist John Hawks, who places the human-chimp divergence at about ten million years ago, but I’ll let that pass for now.

I shall also overlook the fact that Professor Moran severely underestimates the genetic differences between humans and chimps. As Jon Cohen explains in an article in Science (Vol. 316, 29 June 2007) titled, Relative Differences: The Myth of 1%, these differences include “35 million base-pair changes, 5 million indels in each species, and 689 extra genes in humans,” although he adds that many of these may have no functional meaning, and he points out that many of the extra genes in human beings are probably the result of duplication. Cohen comments: “Researchers are finding that on top of the 1% distinction, chunks of missing DNA, extra genes, altered connections in gene networks, and the very structure of chromosomes confound any quantification of ‘humanness’ versus ‘chimpness.’” Indeed, Professor Moran himself acknowledges in another post that “[t]here are about 90 million base pair differences as insertion and deletions (Margues-Bonet et al., 2009),” but he goes on to add that the indels (insertions and deletions) “may only represent 90,000 mutational events if the average length of an insertion/deletion is 1kb (1000 bp).” Still, 90,000 is a pretty small number, compared to his estimate of 22.4 million mutations that have occurred in the human line.

I could also point out that the claim made by Professor Moran that the DNA of humans and chimps is 98.6% identical in areas where it can be aligned is misleading, taken on its own: what it overlooks is the fact that, as creationist geneticist Jeffrey Tomkins (who obtained his Ph.D. from Clemson University) has recently demonstrated, the chromosomes of chimpanzees display “an overall genome average of only 70 percent similarity to human chromosomes” (Human and Chimp DNA–Nearly Identical, Acts & Facts 43 (2)).

I might add (h/t StephenB) that Professor Moran has overlooked the fact that humans have 23 pairs of chromosomes, whereas chimpanzees (and other great apes) have 24. However, Dr. Jeffrey Tomkins has published an article titled, Alleged Human Chromosome 2 “Fusion Site” Encodes an Active DNA Binding Domain Inside a Complex and Highly Expressed Gene—Negating Fusion (Answers Research Journal 6 (2013):367–375). Allow me to quote from the abstract:

A major argument supposedly supporting human evolution from a common ancestor with chimpanzees is the “chromosome 2 fusion model” in which ape chromosomes 2A and 2B purportedly fused end-to-end, forming human chromosome 2. This idea is postulated despite the fact that all known fusions in extant mammals involve satellite DNA and breaks at or near centromeres. In addition, researchers have noted that the hypothetical telomeric end-to-end signature of the fusion is very small (~800 bases) and highly degenerate (ambiguous) given the supposed 3 to 6 million years of divergence from a common ancestor. In this report, it is also shown that the purported fusion site (read in the minus strand orientation) is a functional DNA binding domain inside the first intron of the DDX11L2 regulatory RNA helicase gene, which encodes several transcript variants expressed in at least 255 different cell and/or tissue types. Specifically, the purported fusion site encodes the second active transcription factor binding domain in the DDX11L2 gene that coincides with transcriptionally active histone marks and open active chromatin. Annotated DDX11L2 gene transcripts suggest complex post-transcriptional regulation through a variety of microRNA binding sites. Chromosome fusions would not be expected to form complex multi-exon, alternatively spliced functional genes. This clear genetic evidence, combined with the fact that a previously documented 614 Kb genomic region surrounding the purported fusion site lacks synteny (gene correspondence) with chimpanzee on chromosomes 2A and 2B (supposed fusion sites of origin), thoroughly refutes the claim that human chromosome 2 is the result of an ancestral telomeric end-to-end fusion.

If Professor Moran believes that Dr. Tomkins’ article on chromosome fusion is flawed, then he owes his readers an explanation as to why he thinks so.

The vital flaw in Moran’s reasoning

Leaving aside these points, the real flaw in Professor Moran’s analysis is that he assumes that the essential differences between humans and chimpanzees reside in the 22.4 million-plus mutations – for the most part, neutral or near-neutral – that have occurred in the human line since our ancestors split off from chimpanzees. This is where I must respectfully disagree with him.

In my recent post, Does Professor Larry Moran (or anyone else) understand macroevolution? (March 19, 2014), I wrote:

No scientist can credibly claim to have a proper understanding of macroevolution unless they can produce at least a back-of-the-envelope calculation showing that it is capable of generating new species, new organs and new body plans, within the time available. So we need to ask: is there enough time for macroevolution?

I didn’t ask for a demonstration that macroevolution is capable of generating the neutral or near-neutral mutations that distinguish one lineage from another. Rather, what I wanted was something more specific.

In the post cited above, I endorsed the claim made by Dr. Branko Kozulic, in his 2011 VIXRA paper, Proteins and Genes, Singletons and Species, that the essential differences between species resided not in the neutral mutations they may have accumulated over the course of time, but in the hundreds of chemically unique genes and proteins they possessed, which have no analogue in other species. What Professor Moran really needs to show, then, is that a process of random genetic drift acting on neutral mutations is capable of generating these the chemically unique genes and proteins.

In an article titled, All alone (NewScientist, 19 January 2013), Helen Pilcher (whose hypothesis for the origin of orphan genes I critiqued in my last post) writes:

Curiously, orphan genes are often expressed in the testes – and in the brain. Lately, some have even dared speculate that orphan genes have contributed to the evolution of the biggest innovation of all, the human brain. In 2011, Long and his colleagues identified 198 orphan genes in humans, chimpanzees and orang-utans that are expressed in the prefrontal cortex, the region of the brain associated with advanced cognitive abilities. Of these, 54 were specific to humans. In evolutionary terms, the genes are young, less than 25 million years old, and their arrival seems to coincide with the expansion of this brain area in primates. “It suggests that these new genes are correlated with the evolution of the brain,” says Long.

These are the genes that I’m really interested in. Can a neutral theory of evolution, such as the one espoused by Professor Moran, account for their origin? Creationist geneticist Jeffrey Tomkins thinks not. In a recent blog article titled, Newly Discovered Human Brain Genes Are Bad News for Evolution, he writes:

Did the human brain evolve from an ape-like brain? Two new reports describe four human genes named SRGAP2A, SRGAP2B, SRGAP2C, and SRGAP2D, which are located in three completely separate regions on chromosome number 1.(1) They appear to play an important role in brain development.(2) Perhaps the most striking discovery is that three of the four genes (SRGAP2B, SRGAP2C, and SRGAP2D) are completely unique to humans and found in no other mammal species, not even apes.

Dr. Tomkins then summarizes the evolutionary hypothesis regarding the origin of these genes:

While each of the genes share some regions of similarity, they are all clearly unique in their overall structure and function when compared to each other. Evolutionists claim that an original version of the SRGAP2 gene inherited from an ape-like ancestor was somehow duplicated, moved to completely different areas of chromosome 1, and then altered for new functions. This supposedly occurred several times in the distant past after humans diverged from an imaginary ancestor in common with chimps.

However, this hypothesis faces two objections, which Dr. Tomkins considers fatal:

But this story now wields major problems. First, when compared to each other, the SRGAP2 gene locations on chromosome 1 are each very unique in their protein coding arrangement and structure. The genes do not look duplicated at all. The burden of proof is on the evolutionary paradigm, which must explain how a supposed ancestral gene was duplicated, spliced into different locations on the chromosome, then precisely rearranged and altered with new functions—all without disrupting the then-existing ape brain and all by accidental mutations.

The second problem has to do with the exact location of the B, C, and D versions of SRGAP2. They flank the chromosome’s centromere, which is a specialized portion of the chromosome, often near the center, that is important for many cell nucleus processes, including cell division and chromatin architecture.(3) As such, these two regions near the centromere are incredibly stable and mutation-free due to an extreme lack of recombination. There is no precedent for duplicated genes even being able to jump into these super-stable sequences, much less reorganizing themselves afterwards.

Professor Moran asks some more questions about species

In his latest post, What do Intelligent Design Creationists really think about macroevolution? (March 20, 2014), Professor Moran writes:

I’m not very clear on the "Theory" of Intelligent Design Creationism. Maybe it also predicts what it will be difficult to decide whether Neanderthals and Denisovans are separate species or part of Homo sapiens. Does anyone know how Intelligent Design Creationism deals with these problems? Can it tell us whether lions and tigers are different species or whether brown bears and polar bears are different species?

That’s a fair question, and I’ll do my best to answer it.

(a) Why Modern humans, Neandertals and Denisovans are all one species

Modern humans, Neandertals and Denisovans, who broke off from the lineages leading to Neandertal man and modern man at least 800,000 years ago, are known to have had 23 pairs of chromosomes in their body cells (or 46 chromosomes altogether), as opposed to the other great apes, which have 24 pairs (or 48 altogether).

What’s more, the genetic differences between modern man, Neandertal man and Denisovan man are now known to have been slight – so slight that it has been suggested that they be grouped in one species, Homo sapiens (see here, here, here, here, but see also here).

Finally, Dr. Jeffrey Tomkins addressed the genome of Neandertal man in a 2012 blog post titled, Neanderthal Myth and Orwellian Double-Think (16 August 2012):

Modern humans and Neanderthals are essentially genetically identical. Neanderthals are unequivocally fully human based on a number of actual genetic studies using ancient DNA extracted from Neanderthal remains.

An excursus regarding fruit flies and the identification of species

We noted above that Neandertals and Denisovans (which are all thought to belong to the same species) diverged around 800,000 years ago. However, a recent article by Nicola Palmieri et al., titled, The life cycle of Drosophila orphan genes (eLife 2014;3:e01311, 19 February 2014), indicates that orphan genes have been gained and lost in different species of the fruit-fly genus Drosophila. According to Timetree, Drosophila persimilis and Drosophila pseudoobscura diverged 0.9 million years ago. Drosophila pseudoobscura possesses no less than 228 orphan genes.

It seems prudent to conclude, then, that lineages which are known to have diverged more than 1 million years ago are indeed bona fide species.

N.B. A Science Daily press release at the time of publication of the article makes the following extravagant claim: “Recent work in another group has shown how orphan genes can arise: Palmieri and Schlötterer’s work now completes the picture by showing how and when they disappear.” It appears that this “other group” is actually a group of researchers at the University of California, Davis, who have shown in a recent study that new genes are being continually created from non-coding DNA, more rapidly than expected. Here’s the reference: Li Zhao, Perot Saelao, Corbin D. Jones, and David J. Begun. Origin and Spread of de Novo Genes in Drosophila melanogaster Populations. Science, 2013; DOI: 10.1126/science.1248286. I haven’t read the article, but judging from the press release, it seems that the authors haven’t identified a mechanism for the creation of these genes, as yet: “Zhao said that it’s possible that these new genes form when a random mutation in the regulatory machinery causes a piece of non-coding DNA to be transcribed to RNA.”

Dr. Jeffrey Tomkins provides a hilarious send-up of this logic in his article, Orphan Genes and the Myth of De Novo Gene Synthesis:

The circular form of illogical reasoning for the evolutionary paradigm of orphan genes and its counterpart ‘de novo gene synthesis’, goes like this. Orphan genes have no ancestral sequences that they evolved from. Therefore, they must have evolved suddenly and rapidly from non-coding DNA via de novo gene synthesis. And, are you ready? De novo gene synthesis must be true because orphan genes exist – orphan genes exist because of de novo gene synthesis. As you can see, one aspect of this supports the other in a circular fashion of total illogic – called a circular tautology.

At this stage, I think that press claims that scientists have solved the origin of orphan genes look decidedly premature, to say the least.

(b) Lions, tigers and leopards

What about lions and tigers? According to Timetree, lions and leopards diverged only 2.9 million years ago, while lions and tigers diverged 3.7 million years ago. All of these “big cats” represent different species of the genus Panthera. By comparison, humans and chimps (which are unquestionably different species) are said to have diverged 6.3 million years ago.

A recent article from Nature by Yun Sung Cho et al. (Nature Communications 4, Article number: 2433, doi:10.1038/ncomms3433, published 17 September 2013), titled, The tiger genome and comparative analysis with lion and snow leopard genomes, makes the following observations:

The Amur tiger genome is the first reference genome sequenced from the Panthera lineage and the second from the Felidae species. For comparative genomic analyses of big cats, we additionally sequenced four other Panthera genomes and tried to predict possible big cats’ molecular adaptations consistent with the obligatory meat eating and muscle strength of the predatory Panthera lineage. The tiger and cat genomes showed unexpectedly similar repeat compositions and high genomic synteny, and these indicated strong genomic conservation in Felidae. These results could be supported by the recency of the 37 species-Felidae radiation (<11 MYA)(15) and well-known hybridizations in captivity among subspecies in Felidae lineage such as liger and tigon. By contrast, the ratio of repeat components for the great apes was considerably different among species, especially between human and orang-utan(28), which diverged about the same time as felines. The breaks in synteny that we observed are likely occasional rare sporadic exchanges that accumulated over this short period (<11 MYA) of evolutionary time. The paucity of exchanges across the mammalian radiations (by contrast to more reshuffled species such as Canidae, Gibbons, Ursidae and New World monkeys) is a hallmark of evolutionary constraints.

Figure 1b in the article reveals that tigers have certain genes which cats lack. However, I was unable to ascertain whether tigers had any chemically unique orphan genes that lions or leopards lacked.

A Science Daily report titled, Tiger genome sequenced: Tiger, lion and leopard genomes compared (September 20, 2013) which discussed the findings in the above-cited article, added the following information:

Researchers also sequenced the genomes of other Panthera-a white Bengal tiger, an African lion, a white African lion, and a snow leopard-using next-gen sequencing technology, and aligned them using the genome sequences of tiger and domestic cat. They discovered a number of Panthera lineage-specific and felid-specific amino acid changes that may affect the metabolism pathways. These signals of amino-acid metabolism have been associated with an obligatory carnivorous diet.

Furthermore, the team revealed the evidence that the genes related to muscle strength as well as energy metabolism and sensory nerves, including olfactory receptor activity and visual perception, appeared to be undergoing rapid evolution in the tiger.

I should add that although lions and tigers can interbreed, the offspring (ligers and tigons) are nearly always sterile, because the parent species have different numbers of chromosomes.

From the above evidence, it appears likely that lions, tigers and leopards are genuinely different species, and that each species was intelligently engineered.

(c) Brown bears and polar bears

The case of brown bears and polar bears is much more difficult to decide, as there appear to be no online articles on orphan genes in these animals. However, Timetree indicates that they diverged 1.2 million years ago, which is a little earlier than the time when Drosophila persimilis and Drosophila pseudoobscura diverged (0.9 million years ago). It therefore seems likely that these two bears belong to different species.

Conclusion

I shall stop there for today. In conclusion, I’d like to point out that Professor Moran nowhere addressed the problem of the origin of orphan genes in his reply, so he didn’t really answer the first argument in my previous post, which was that we cannot claim to understand macroevolution until we ascertain the origin of the hundreds of chemically unique proteins and orphan genes that characterize each species.

To Professor Moran’s credit, he did attempt to answer my second argument (why is there so much stasis in the fossil record?), by suggesting that even large populations will still change slowly in their diversity, as new alleles increase in frequency and old ones are lost, but that morphological change is “more likely to occur during speciation events when the new daughter population (species) is quite small and rapid fixation of rare alleles is more likely.” But as I argued previously, why, during the times of environmental upheaval described by Professor Prothero, don’t we see a diversification of niches? Why don’t species branch off? Why do we instead see morphological stasis persisting for millions of years? That remains an unsolved mystery.

Finally, it seems to me that Professor Moran has solved the “time” question (my third argument) only in a trivial sense: he has calculated that the requisite number of mutations separating humans and chimps could have gotten fixed in the human line. I have to say I found his claim that in the last five million years, 22.4 million mutations have become fixed in the lineage leading to human beings, utterly astonishing. But even supposing that this figure is correct, what it overlooks is that the mutations accounting for the essential differences between humans and chimps aren’t your ordinary, run-of-the-mill mutations. Many of them seem to have involved orphan genes, which means that until we can explain how these genes arise, we lack an adequate account of macroevolution.

117 Replies to “So, why are the human and chimpanzee/bonobo genomes so similar? A reply to Professor Larry Moran

  1. 1
    scordova says:

    who obtained his Ph.D. from Clemson University)

    That understates his qualifications a little. He also became a Clemson faculty member and ran a genetics center and was a reviewer of peer-reviewed genetics papers in the secular world.

    He’s very qualified to criticize and reject papers by evolutionists. He’s just doing his rejection publicly now. If he disagrees with the numbers being provided by evolutionists, he shouldn’t be considered the outlier, they should be.

    He demonstrated quite well their methods were sampling the 98% that was 98% similar so of course you get 98% identity.

    I wrote of my encounter with Tomkins here:
    Jeff Tomkins vs Evolutionary biologist who got laughed off stage

    As far as Moran’s numbers, of course they’ll match up! The circularly reasoned mutation rate is reasoned based on the divergence amount and the supposed time of a split. Because of Kimura’s formula highlighted here:

    If not Rupe or Sanford

    the number fixed will always agree with the circularly reasoned mutation rate. It’s circular reasoning pretending to make a prediction when in fact it’s a post diction. But this is all circular reasoning.

    Or maybe the IDiots have a good explanation that they haven’t revealed?

    No Moran, you’re the …… for not recognizing circular reasoning. You can take a tree and a frog, make up a timeline and you’ll never get inconsistent results as long as the mutation rates being used are the circularly reasoned ones and not the actual field-measured ones (which are too expensive for anyone to do right now)! The fixation rate will always match the circularly-reasoned mutation rate. The way to settle the issue is to use real-time mutation rates, but that is too expensive right now.

    Tomkins is right to point out, doing the Chimp genome right is not being done for whatever reason. Is it that it would overturn a narrative? 🙂

    The real problem is how the human genome could tolerate such variability. As Kondrashov pointed out, “why aren’t we dead 100 times over!”

    PS

    To help you understand a little more:

    If the effective population was 10,000, and a gametic mutation rate of 100 per individual, that means there are

    10,000 * 100 = 1,000,000

    new mutations in the pool for that generation.

    From this pool of 1,000,000, 100 will go to fixation, or 1 out of 10,000 from the entire pool of 1 million.

    Thus a mutation rate of 100 yields a fixation rate of 100 even though 99.9% of the mutants disappear due to drift.

  2. 2
    Robert Byers says:

    Should write a book sir! I guess the internet in effect is books. Anyways.

    Human/chimp thing is entirely based on looks equals like descent. A line of reasoning. If DNA is invoked its the same line of reasoning. Same looks equals same DNA equals same common descent.
    All mere reasoning without scientific investigation demonstrating common descent.
    They add a few details.

    This YEC says it could only be we look like chimps.
    Primates have the best bodies for a human made in Gods image/intelligence to use and have fun in. What other body type on earth would be better? name it!

    Since we must be in the spectrum of nature. bum, legs, liver, eyes then HOW could a special being , made like gOD, find a identity in our own body unique from others?
    We couldn’t. Even our hearts in our backs wouldn’t do it.
    therefore we uniquely DO NOT have our own body representing our identity. animals do.
    We are borrowing the best type of body that was in the spectrum of biology.
    A line of reasoning to replace other lines of reasoning.
    Evolutionists do not have scientific evidence for human/chimp common descent but simply a likeness hunch persudes them in the quiet of the night.

  3. 3
    Graham2 says:

    Wood feels compelled to reject common ancestry, since he believes the Bible clearly teaches the special creation of human beings

    Religion poisons everything.

  4. 4

    I think the 1% argument is ridiculous especially in light of knowing the 23 vs 24 chromosome pair difference. I also have never seen a good argument going from 24 to 23 chromosome pairs. So one “ancestor” develops the fused chromosome and then mates with some other animal with 24 chromosomes and then a pair is lost and the fused chromosome duplicates and passed on and then dominates a whole population within how much time? It is also interesting to look at the recent advances in the field “omics” as they are now looking at not only genomics, but proteonomics, and metabonomics. This plus all the epigenetic mechanisms we know of as well. For each gene change there comes a multitude of other changes that do not come with a free lunch

  5. 5

    I think the 1% argument is ridiculous especially in light of knowing the 23 vs 24 chromosome pair difference. I also have never seen a good argument going from 24 to 23 chromosome pairs. So one “ancestor” develops the fused chromosome and then mates with some other animal with 24 chromosomes and then a pair is lost and the fused chromosome duplicates and passed on and then dominates a whole population within how much time? It is also interesting to look at the recent advances in the field “omics” as they are now looking at not only genomics, but proteonomics, and metabonomics. This plus all the epigenetic mechanisms we know of as well. For each gene change there comes a multitude of other changes that do not come with a free lunch

  6. 6
    Mapou says:

    vjtorley:

    1. Personally, I accept the common ancestry of humans, chimpanzees and bonobos. Of course, I am well aware that many Intelligent Design theorists don’t accept common ancestry, but some prominent ID advocates do. Why do I accept common descent? Because I think it’s the best explanation for the pattern of similarities we find between humans, chimpanzees and bonobos.

    Nice post. However, I don’t see why similarity in design necessarily implies common descent. If an architect designs two slightly dissimilar buildings one after the other, where is the common descent in this process? I am assuming that by common descent, one means that the species arose via a long sequence of sexual reproduction events acted upon by random variations.

    As a software engineer, I know I don’t use any kind of sexual reproduction mechanism to derive one class of objects from another. Why could not the designers have a huge database of pre-designed genes to choose from and with which to create new species of animals and humans? And why would they need sexual reproduction to accomplish this? Beings that advanced could easily incubate newly designed species outside the womb, no?

  7. 7
    Mapou says:

    Let me add that, as a Christian, I am proud and happy to be genetically related to chimps and bonobos. They are awesomely complex and wonderfully designed creatures.

  8. 8
    wallstreeter43 says:

    being similar and being related are 2 different things. There are many reasons why I dont accept common ancestry and one of them being that we dont see true transitionary charts in the fossil records but leaps from fully formed animals to fully formed animals.

    Now the designer could have added genes to one animal in effect turning it into another but that wouldnt be evolution, that would be the work of a creator with a great imagination.

    It is this leap of information that makes me sketical of common descent.

  9. 9
    Roy says:

    Professor Moran makes the remarkable claim that 130 mutations are fixed in the human population, in each generation. Here are a few reasons why I’m doubtful, even after reading his posts on the subject (see here, here and here):

    (a) most mutations will be lost due to drift, so a mutation will have to appear many times before it gets fixed in the population;
    (b) necessarily, the mutation rate will always be much greater than the fixation rate;
    (c) nearly neutral mutations cannot be fixed except by a bottleneck.

    I owe the above points to a skeptical biologist who kindly offered me some advice about fixation. As I’m not a scientist, I shall pursue the matter no further. Instead, I’d like to invite other readers to weigh in. Is Professor Moran’s figure credible?

    Yes.

    The probability of any given allele eventually reaching fixation is equal to it’s frequency in the population, so the probability of any single mutation reaching fixation in a population is 1/N, where N is the population size. Your point (c) is demonstrably incorrect both mathematically and by simulation. Your point (a) is also incorrect. Those very few mutations that do reach fixation through drift do not need to have occurred multiple times, though given the size of the human population compared with the size of our genome they may well have done so. Your point (b) is correct, but only if comparing the fixation rate with the mutation rate across the whole population, since the fixation rate is the same as the mutation rate for an individual:

    m mutations per individual -> m*N mutations per generation -> m*N/N mutations per generation that will become fixed -> m mutations fixed per generation. Our population size means that those mutations happening now will take a very long time to reach fixation, and only 1 in 6000000000 will achieve it, and the current population increase means that there is a temporary slowdown in fixation rates, but that has not applied over most of the last few million years and as can be seen from the above calculation the fixation rate throughout a population is effectively independent of population size.

    Professor Moran is also assuming that chimps and humans diverged a little over five million years ago. He might like to read the online articles, What is the human mutation rate? (November 4, 2010) and A longer timescale for human evolution (August 10, 2012), by paleoanthropologist John Hawks, who places the human-chimp divergence at about ten million years ago, but I’ll let that pass for now.

    I won’t. Doubling the timescale doubles the number of mutations fixed and eliminates any problem.

    Finally (emphasis mine):

    I shall also overlook the fact that Professor Moran severely underestimates the genetic differences between humans and chimps. As Jon Cohen explains in an article in Science (Vol. 316, 29 June 2007) titled, Relative Differences: The Myth of 1%, these differences include “35 million base-pair changes, 5 million indels in each species, and 689 extra genes in humans,” … his [Moran’s] estimate of 22.4 million mutations that have occurred in the human line.

    22.4 million mutations could easily produce 5 million indels, 35 million base pair changes and 689 new genes. How is it a severe underestimate?

    Roy

  10. 10
    Joe says:

    I don’t accept universal common descent because it cannot be scientifically tested.

    Also, contra Moran, we don’t know anything about fixation rates. And similarities can easily be explained by a common design.

  11. 11
    Charles says:

    vjtorley in OP:

    “Why would a Designer do it that way?” you ask. “Why not just make a human being in a single step?” The short answer is that the Designer wasn’t just making human beings, but the entire panoply of life-forms on Earth, including all of the great apes. … If we suppose that the Designer operates according to a “minimum effort” principle, then successive tweakings would have been the way to go.

    We should not ignore that the “single step” resulting in the simultaneous or concurrent emergence of humans and all great apes presupposes life-sustainable environments without deleterious competition/encroachment. While early humans were more fragile and intelligent and could not survive marauding hordes of apes, yet great apes could not survive modern intelligent human predation/encroachment. Maybe time was required for ecological niches to be established such that all survive. Possibly there are other factors as well.

    The Designer, like a good engineer, not only seeks elegant efficiency but also shared survivability.

  12. 12
    jw777 says:

    I am reminded of my first compare-and-contrast assignment in kindergarten.

    Simply, if you look to showcase similarities through comparison, you should not be surprised to find out that you have enumerated a great many similarities. This is no more sophisticated than Stuart Smalley beginning with positive affirmations only to find he feels “good enough” afterwards.

    The very damning fact remains that what we are really talking about here is an actual infinitesimally small comparative, which means an infinite contrast. My body is made of 100 trillion bacteria. The “human” cells number only 1 trillion. When looking at the genome of the cells, we have historically ignored 99% of the code. Within the 1% that we have paid any attention to, we didn’t know about its second layer of code (Duons) until a few months ago. So, 1% of one layer of the genetic code for our cells is 98% similar to 1% of one layer of genetic code for chimp cells. Ouch. Now pay very close attention: My biological makeup is AT MOST 0.000049% similar to chimps. That is neither a strong case for common descent or common design.

    Can we put this parochial exercise behind us yet? If chimps meant anything at all, we wouldn’t be spending all of our pre-human medical trial dollars on rat testing; nor would our best non-human research of problem solving be based on crows; nor would our best non-human research of language be looking at bees and mollusks.

    This shouldn’t even be a discussion among academics. If you tally the quantitative genetic differences, and factor the qualitative epigenetic and trait differences, you find that a comparison of primates is a convoluted and laughable exercise in placebo effect. Please, let us remove the smoke AND the mirrors.

  13. 13
    Timmy says:

    The only way common descent can be an explanation (for similarities, or anything) is if the organisms have all the same integrated systems and structures and the only differences are in fundamentally irrelevant mutations.

    However small the differences between chimps and humans, it remains that they are clearly not small enough for evolution to have produced them.

    And even if common descent becomes legitimate, I don’t understand why it is preferable to the “lazy designer” explanation, since the two are indistinguishable in this case.

    Could someone help me out?

  14. 14
    vjtorley says:

    Hi Sal and Roy,

    Thanks for the mathematical exposition. I think I can understand the logic now; I wish Professor Moran had explained it in the posts I cited, as you both did. All the same, I would like to see an actual measurement of the rate of fixation in the human population over (say) the last 200 years, confirming the calculated rate.

    By the way, Roy, I think I made it clear that indels would significantly alter the number of base pairs, but would have little effect on the number of mutations. Finally, as I said, the critical question we need to examine is whether unguided processes can account for the orphan genes in the human genome.

    FYI: http://creation.com/from-ape-t.....-in-crisis Thoughts?

  15. 15
    drc466 says:

    Oddly, as a YEC one of the points I object to most is the stolen base Creationist Todd Wood grants the evolutionist in your post above: that somehow, common design (morphology) is NOT sufficient reason to expect significant genetic similarity.

    A very popular argument is that similarity does not necessarily indicate common ancestry but could also imply common design (e.g. Batten 1996; Thompson and Harrub 2005; DeWitt 2005).

    A most reasonable question is that, given the morphological similarities, would you expect the genome to be MORE or LESS similar if humans and chimps don’t have common ancestry? I would argue that the genome shows greater difference than one would expect just based on physical similarities, without regard to common ancestry.

    As an example consider a 200,000 nucleotide region from human chromosome 1 (Figure 2). When compared to the chimpanzee, the two species differ by as little as 1-2%, …

    Considering that chromosome 1 spans 249 Million nucleotide base pairs, this is like finding 2 sentences in the works of Shakespeare that match 2 sentences in the works of Jane Austen closer than they match the works of Tolstoy. What happens to that % if we double that 200,000 to 400,000? or 2,000,000?

    …but when compared to the mouse, the differences are much greater. Comparison to chicken reveals even greater differences.

    Again – based purely on morphology, would we not expect this to be true? Why does common ancestry add anything to the argument? Is there some rule somewhere that says if God created man separately, He has to use completely different genetic coding? That’s ridiculous.

    This is exactly the expected pattern of similarity that would result if humans and chimpanzees shared a recent common ancestor and mice and chickens were more distantly related.

    And the expected pattern if they were created. If explanation a is not greater than explanation b, there is no reason to accept a over b.

    The question is not how similarity arose but why this particular pattern of similarity arose. To say that God could have created the pattern is merely ad hoc.

    Faulty assertion. To say that God HAD TO CHANGE THE PATTERN is merely ad hoc.

    The specific similarity we observe between humans and chimpanzees is not therefore evidence merely of their common ancestry but of their close relationship.

    No – it is evidence of their close morphology. Why is this difficult to understand/accept?

    It’s overkill to apply the same analysis to the rest of the quote, but I’d like to touch on one more:

    They found that the open reading frame of 33 of the human genes were interrupted by nonsense codons or deletions, rendering them pseudogenes.

    Really? I’d be willing to bet that, if you randomly mutated ALL “nonsense codons or deletions” in an evolutionist’s genome, they would immediately and promptly die. Any takers?

    Finally – I fear Mr. Wood has chosen to take an oddly pro-evolutionary stance in his paper that is at odds with his stated pro-creation views. Some of his statements are, honestly, difficult to understand. For example:

    An insertion or deletion of 1000 nucleotides is only one mutational event, even though the total difference is 1000 nucleotides.

    As far as I know, this is a purely hypothetical assertion that is quite difficult to accept. Here he is arguing that a 1000-nucleotide mutation is a) a single point mutation that b) manages to “stick” in the entire species despite c) being probabilistically neutral or deleterious.
    The reason to not accept human/chimp/bonobo similarity as proof of common ancestry is that:
    1) It adds no explanatory power above common morphology (aka design)
    2) Genomic similarity is arguably significantly less than would be expected by common ancestry. If human/ape similarity were 99% without the use of dictionary tricks (i.e. same number of chromosomes, same number of genes, less than 1% difference in length, out of every 1million nucleotides 990000 nucleotides matched), then common ancestry would be the better explanation
    3) The Bible clearly teaches Creation. On this much Mr, Wood and I agree.

  16. 16
    drc466 says:

    One question Todd Wood asks that I think is a very good one, and goes to the root of Dr. Moran’s argument, is this:

    The question remains as to why God created an animal that is so similar to humans.

    Personally, my response would be that it helps to emphasize how humans are different. Man being created “in the image of God” is not talking about physically similarity, and because we have apes, and chimps, and bonobos, we know that clearly. How would we view ourselves as creations of God differently, if chimps and bonobos didn’t exist?
    Another possible reason would be, perhaps, free will and faith. If man were, for example, the only mammal, would it be possible to be an “intellectually fulfilled atheist”? Would God be cheating?

  17. 17
    HD says:

    Hi VJ

    A couple of questions for you please.

    1. You admit to believing in common descent yet spend the post arguing about specific scientific evidence. What’s the point? Are you just arguing for him to find better evidence for common descent – even though you admitted to the evidence that HAS made you a believer? I mean, in the end, you both believe in the common descent issue yet for different reasons.

    2. What would you say about Casey Luskin’s post here:

    http://www.evolutionnews.org/2.....83331.html

    that brings up a bunch of stuff AGAINST common descent (even though he says it MIGHT be true). You seem to be convinced by the most obvious pieces of evidence that has convinced me. What do you say about the counter arguments Mr. Luskin brings up?

    thank you
    HD

  18. 18
    gpuccio says:

    HD:

    I would like to say that there are very good arguments in favor of universal common descent, and there are also very good arguments against it. That should not be a surprise. Scientific knowledge is not easy, and apparent contradictions are often a good clue to new understanding.

    I accept, at present, common descent as the best available explanation for the majority of empirical observations. I agree with VJ, and Behe, and others, on that point. But I respect those who have a different judgement, and remain wholly open to new evaluations.

    My personal worldview is that our religious convictions should not consciously influence our scientific judgements (they will certainly do that subconsciously, because cognitive bias cannot be eliminated in human experience). Therefore, I am not a creationist, in the sense that I have no desire to use science to justify my religious convictions.

    That said, I respect those who think differently.

  19. 19
    Roy says:

    By the way, Roy, I think I made it clear that indels would significantly alter the number of base pairs, but would have little effect on the number of mutations.

    Yes, but you didn’t make it clear how Moran severely underestimated the genetic distance between humans and chimps.

    Finally, as I said, the critical question we need to examine is whether unguided processes can account for the orphan genes in the human genome.

    FYI: http://creation.com/from-ape-t…..-in-crisis Thoughts?

    I’ve examined some of Sanford’s work before – his Mendel’s accountant simulation – and found it to incorporate so many biased assumptions it’s beyond useless.

    Roy

  20. 20
    bornagain77 says:

    Roy you state,

    I’ve examined some of Sanford’s work before – his Mendel’s accountant simulation – and found it to incorporate so many biased assumptions it’s beyond useless.

    Now this is a particularly interesting accusation for you, a Darwinist, to make, since Darwinists are notorious for smuggling in information into their evolutionary algorithms (i.e. Dawkins’ targeted Weasel phrase). Algorithms that they have, get this, ‘Intelligently Designed’ to prove that Intelligence is not necessary for the generation of information. 🙂 Myself, I have found Sanford and company’s ‘assumptions’ to be overly generous to Darwinian presuppositions. And even with the overly generous assumptions granted to Darwinian processes the program still found Darwinian processes to be grossly inadequate to account for the information we find in life:

    Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory – 2008
    Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue.
    Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person.
    http://www.icr.org/i/pdf/techn.....Theory.pdf

    Using Numerical Simulation to Better Understand Fixation Rates, and Establishment of a New Principle – “Haldane’s Ratchet” – Christopher L. Rupe and John C. Sanford – 2013
    Excerpt: We then perform large-scale experiments to examine the feasibility of the ape-to-man scenario over a six million year period. We analyze neutral and beneficial fixations separately (realistic rates of deleterious mutations could not be studied in deep time due to extinction). Using realistic parameter settings we only observe a few hundred selection-induced beneficial fixations after 300,000 generations (6 million years). Even when using highly optimal parameter settings (i.e., favorable for fixation of beneficials), we only see a few thousand selection-induced fixations. This is significant because the ape-to-man scenario requires tens of millions of selective nucleotide substitutions in the human lineage.
    Our empirically-determined rates of beneficial fixation are in general agreement with the fixation rate estimates derived by Haldane and ReMine using their mathematical analyses. We have therefore independently demonstrated that the findings of Haldane and ReMine are for the most part correct, and that the fundamental evolutionary problem historically known as “Haldane’s Dilemma” is very real.
    Previous analyses have focused exclusively on beneficial mutations. When deleterious mutations were included in our simulations, using a realistic ratio of beneficial to deleterious mutation rate, deleterious fixations vastly outnumbered beneficial fixations. Because of this, the net effect of mutation fixation should clearly create a ratchet-type mechanism which should cause continuous loss of information and decline in the size of the functional genome. We name this phenomenon “Haldane’s Ratchet”.
    http://media.wix.com/ugd/a704d.....fa9c20.pdf

    It is interesting to note how reluctant some Darwinists are to divulge their programs:

    Calling all Darwinists, where is your best population genetics simulation? – September 12, 2013
    Excerpt: So Darwinists, what is your software, and what are your results? I’d think if evolutionary theory is so scientific, it shouldn’t be the creationists making these simulations, but evolutionary biologists! So what is your software, what are your figures, and what are your parameters. And please don’t cite Nunney, who claims to have solved Haldane’s dilemma but refuses to let his software and assumptions and procedures be scrutinized in the public domain. At least Hey was more forthright, but unfortunately Hey’s software affirmed the results of Mendel’s accountant.
    http://www.uncommondescent.com.....imulation/

    A few notes as to the ‘hidden assumptions’ of Darwinists smuggled into Evolutionary Algorithms:

    “The computer is not going to generate anything realistic if it uses Darwinian mechanisms.”
    Dr. David Berlinski: Accounting for Variations – video
    http://www.youtube.com/watch?v=aW2GkDkimkE

    LIFE’S CONSERVATION LAW – William Dembski – Robert Marks – Pg. 13
    Excerpt: Simulations such as Dawkins’s WEASEL, Adami’s AVIDA, Ray’s Tierra, and Schneider’s ev appear to support Darwinian evolution, but only for lack of clear accounting practices that track the information smuggled into them.,,, Information does not magically materialize. It can be created by intelligence or it can be shunted around by natural forces. But natural forces, and Darwinian processes in particular, do not create information. Active information enables us to see why this is the case.
    http://evoinfo.org/publication.....ation-law/

    Conservation of Information Made Simple – William A. Dembski – August, 2012
    Excerpt: Biological configuration spaces of possible genes and proteins, for instance, are immense, and finding a functional gene or protein in such spaces via blind search can be vastly more improbable than finding an arbitrary electron in the known physical universe. ,,,
    ,,,Given this background discussion and motivation, we are now in a position to give a reasonably precise formulation of conservation of information, namely: raising the probability of success of a search does nothing to make attaining the target easier, and may in fact make it more difficult, once the informational costs involved in raising the probability of success are taken into account. Search is costly, and the cost must be paid in terms of information. Searches achieve success not by creating information but by taking advantage of existing information. The information that leads to successful search admits no bargains, only apparent bargains that must be paid in full elsewhere.
    http://www.evolutionnews.org/2.....63671.html

    Before They’ve Even Seen Stephen Meyer’s New Book, Darwinists Waste No Time in Criticizing Darwin’s Doubt – William A. Dembski – April 4, 2013
    Excerpt: In the newer approach to conservation of information, the focus is not on drawing design inferences but on understanding search in general and how information facilitates successful search. The focus is therefore not so much on individual probabilities as on probability distributions and how they change as searches incorporate information. My universal probability bound of 1 in 10^150 (a perennial sticking point for Shallit and Felsenstein) therefore becomes irrelevant in the new form of conservation of information whereas in the earlier it was essential because there a certain probability threshold had to be attained before conservation of information could be said to apply. The new form is more powerful and conceptually elegant. Rather than lead to a design inference, it shows that accounting for the information required for successful search leads to a regress that only intensifies as one backtracks. It therefore suggests an ultimate source of information, which it can reasonably be argued is a designer. I explain all this in a nontechnical way in an article I posted at ENV a few months back titled “Conservation of Information Made Simple” (go here). ,,,

    ,,, Here are the two seminal papers on conservation of information that I’ve written with Robert Marks:
    “The Search for a Search: Measuring the Information Cost of Higher-Level Search,” Journal of Advanced Computational Intelligence and Intelligent Informatics 14(5) (2010): 475-486
    “Conservation of Information in Search: Measuring the Cost of Success,” IEEE Transactions on Systems, Man and Cybernetics A, Systems & Humans, 5(5) (September 2009): 1051-1061
    http://www.evolutionnews.org/2.....70821.html

    supplemental note to Dawkins’ infamous Weasel program where he smuggled in a target phrase to the search:

    A Meaningful World: How the Arts and Sciences Reveal the Genius of Nature – Book Review
    Excerpt: They focus instead on what “Methinks it is like a weasel” really means. In isolation, in fact, it means almost nothing. Who said it? Why? What does the “it” refer to? What does it reveal about the characters? How does it advance the plot? In the context of the entire play, and of Elizabethan culture, this brief line takes on significance of surprising depth. The whole is required to give meaning to the part.
    http://www.thinkingchristian.n.....821202417/

    In fact it is interesting to note what the overall context is for “Methinks it is like a weasel” that is used in the Hamlet play. The context in which the phrase is used is to illustrate the spineless nature of one of the characters of the play. To illustrate how easily the spineless character can be led to say anything that Hamlet wants him to say:

    Ham. Do you see yonder cloud that ’s almost in shape of a camel?
    Pol. By the mass, and ’t is like a camel, indeed.
    Ham. Methinks it is like a weasel.
    Pol. It is backed like a weasel.
    Ham. Or like a whale?
    Pol. Very like a whale.
    http://www.bartleby.com/100/138.32.147.html

    After realizing what the context of ‘Methinks it is like a weasel’ actually was, I remember thinking to myself that that phrase was perhaps the worse possible phrase Dawkins could have possibly chosen to use to try to illustrate his point, since the phrase, when taken into context, actually illustrates that the person saying it (Hamlet) was shamelessly manipulating the other character into saying that a cloud looked like a weasel. Which I am sure is hardly the idea, i.e. deception and manipulation, that Dawkins was trying to convey with his ‘Weasel’ example.

  21. 21
    Evolve says:

    VJTorley,

    Recent paper reporting de novo gene synthesis from non-coding DNA:

    http://www.sciencemag.org/content/343/6172/769

    Reviews on the evolutionary origin of orphan genes:

    http://onlinelibrary.wiley.com.....24601/full

    http://www.nature.com/nrg/jour.....g3053.html

    Orphan genes are not magically created by the creator, Mr. Torley.

  22. 22
    Joe says:

    Roy,

    Why do use equations that no one has ever verified? The point being is no one knows how fast or slow mutations reach fixation- or even if they do in a blind watchmaker scenario.

  23. 23
    Joe says:

    Evolve@ 21- Those papers are speculation and have nothing to do with any mechanism. They definitely do NOT demonstrate blind watchmaker evolution producing novel genes.

  24. 24
    Evolve says:

    Joe@ 23,

    Nice try. But there’s no escaping the evidence. The Science paper did RNA-seq on the testis transcriptome of few D. melanogaster strains and identified several newly-transcribed genes which were absent from the D. melanogaster reference sequence. A sequence alignment showed that these new genes corresponded to intergenic regions in the D. melanogaster reference sequence and orthologous regions of closely related species such as D. simulans & D. yakuba.
    This clearly shows that new genes can arise by mutations in previously non-expressed DNA and it contributes to speciation.
    Now you guys can go on denying everything as you normally do, but nobody is going to take you seriously.

  25. 25
    bornagain77 says:

    Orphan Genes (And the peer reviewed ‘non-answer’ from Darwinists) – lifepsy video
    http://www.youtube.com/watch?v=1Zz6vio_LhY

    Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references
    http://www.vimeo.com/17135166

    Estimating the size of the bacterial pan-genome – Pascal Lapierre and J. Peter Gogarten – 2008
    Excerpt: We have found greater than 139 000 rare (ORFan) gene families scattered throughout the bacterial genomes included in this study. The finding that the fitted exponential function approaches a plateau indicates an open pan-genome (i.e. the bacterial protein universe is of infinite size); a finding supported through extrapolation using a Kezdy-Swinbourne plot (Figure S3). This does not exclude the possibility that, with many more sampled genomes, the number of novel genes per additional genome might ultimately decline; however, our analyses and those presented in Ref. [11] do not provide any indication for such a decline and confirm earlier observations that many new protein families with few members remain to be discovered.
    http://www.paulyu.org/wp-conte.....genome.pdf

    Moreover ‘new’ ORFan genes are found to be just as essential as ‘old’ genes for embryological development, which is completely contrary to evolutionary thought:

    Age doesn’t matter: New genes are as essential as ancient ones – December 2010
    Excerpt: “A new gene is as essential as any other gene; the importance of a gene is independent of its age,” said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. “New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked.”
    http://www.sciencedaily.com/re.....142523.htm

    New genes in Drosophila quickly become essential. – December 2010
    Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages.
    http://www.sciencemag.org/cont.....2.abstract

    Darwinists, either ignorantly or willfully, ignore the brick wall barrier that the de novo creation of just one gene presents for Darwinian processes:

    Could Chance Arrange the Code for (Just) One Gene?
    “our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236).”
    http://www.creationsafaris.com/epoi_c10.htm

    The Extreme Complexity Of Genes – Dr. Raymond G. Bohlin – video
    http://www.metacafe.com/watch/8593991/

    “Is it really credible that random processes could have constructed a reality, the smallest element of which—a functional protein or gene— is complex beyond our own creative capacities, a reality which is the very antithesis of chance, which excels in every sense anything produced by the intelligence of man?”
    ~ Michael Denton

    And though neo-Darwinists like to claim that they have evidence for the origin of new genes, the fact is that it all turns out to be deceptive bluff and bluster on their part:

    Hopeless Matzke -David Berlinski & Tyler Hampton August 18, 2013
    http://www.evolutionnews.org/2.....75631.html

    In fact, direct observational evidence from the lab has yet to show the fixation of ‘unconditionally advantageous alleles’ for fruit flies much less the creation of a new gene in fruit flies:

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies

  26. 26
    bornagain77 says:

    speaking of fruit flies, I found this following recent study to be devastating to evolutionary thought:

    Study of complete RNA collection of fruit fly uncovers unprecedented complexity – March 17, 2014
    Excerpt: Scientists from Indiana University are part of a consortium that has described the transcriptome of the fruit fly Drosophila melanogaster in unprecedented detail, identifying thousands of new genes, transcripts and proteins.
    In the new work, published Sunday in the journal Nature, scientists studied the transcriptome — the complete collection of RNAs produced by a genome — at different stages of development, in diverse tissues, in cells growing in culture, and in flies stressed by environmental contaminants. To do so, they used contemporary sequencing technology to sequence all of the expressed RNAs in greater detail than ever before possible.
    The paper shows that the Drosophila genome is far more complex than previously suspected and suggests that the same will be true of the genomes of other higher organisms. The paper also reports a number of novel, particular results:,,, “splicing factors” (proteins that control the maturation of RNAs by splicing) are themselves spliced in complex ways; and that the Drosophila transcriptome undergoes large and interesting changes in response to environmental stresses.,,,
    “As usual in science, we’ve answered a number of questions and raised even more. For example, we identified 1,468 new genes, of which 536 were found to reside in previously uncharacterized gene-free zones.” “We think these results could influence gene regulation research in all animals,”,,,
    An example they pointed to was the perturbation experiments that identified new genes and transcripts. New genes were identified in experiments where adults were challenged with heat shock, cold shock, exposure to heavy metals, the drug caffeine and the herbicide paraquat, while larvae were treated with heavy metals, caffeine, ethanol or the insecticide rotenone.
    Those environmental stresses resulted in small changes in expression level at thousands of genes; and in one treatment, four newly modeled genes were expressed altogether differently. In total, 5,249 transcript models for 811 genes were revealed only under perturbed conditions.
    http://news.indiana.edu/releas.....ered.shtml

  27. 27
    Joe says:

    Evolve- There isn’t anything in those papers that say blind watchmaker evolution did it. You do realize tat ID is not anti-evolution, right?

  28. 28
    drc466 says:

    Evolve,

    Seriously? From the summary…

    In order to better understand the process by which de novo genes originate, Zhao et al. (p. 769, published online 23 January) examined testis-based gene expression among Drosophila melanogaster strains and identified both fixed and polymorphic de novo genes. The results suggest that spontaneous activation of previously noncoding DNA may be an important factor in generating genetic novelty.

    So, they’ve identified all possible types of genes, fixed, changing, and non-existent. They recognize the results are inconclusive (“suggest”), and that it is not the whole story in any case (“factor”).

    We need to get you a dictionary, mate. 🙂

  29. 29
    Joe says:

    If it takes 25 million years just to get two specific mutations to form a binding site for a gene, how long would it take to produce a new gene, binding site and promoter?

    waiting for two mutations

  30. 30
    Evolve says:

    VJTorley,

    ///If Professor Moran believes that Dr. Tomkins’ article on chromosome fusion is flawed, then he owes his readers an explanation as to why he thinks so.///

    Quoting from the following article:

    http://www.motherjones.com/pol.....-evolution

    Tomkins naturally finds all kinds of supposed problems with the genetic evidence; perhaps his biggest claim is that at the alleged site on human chromosome 2 where the fusion occurred, there’s actually a functioning gene, rather than the remnants of fused telomeres.

    But that’s just wrong, according to Miller. The fusion site is “more than 1,300 bases away from the gene,” he says, based on a review of major gene databanks. “These increasingly desperate efforts to ‘debunk’ the chromosome 2 story have failed before, and they’ve failed this time, too,” Miller concludes.

  31. 31
    gpuccio says:

    Evolve:

    The abstract of the article you quote:

    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.

    So, IOWs, new genes appear from non coding, unexpressed DNA. Exactly. And how do they appear? By mutations. Exactly.

    And so? You comment:

    “This clearly shows that new genes can arise by mutations in previously non-expressed DNA and it contributes to speciation.”

    Exactly. Again, and so?

    I don’t understand what you think that VJ (or I, or other IDists) believe. VJ has clearly stated that he believes in common descent. I have done the same here at #18. Joe has clearly stated, at #27:

    “Evolve- There isn’t anything in those papers that say blind watchmaker evolution did it. You do realize tat ID is not anti-evolution, right?”

    Have you problems in understanding what others say?

    So, you realize that the paper tells us nothing about the mechanism of mutation, don’t you? You realize that according to this scenario the new gene should have evolved by RV alone, without any help from NS, at least until the new gene is ready and functional, don’t you? You realize that an unexpressed segment of DNA cannot be selected for function, don’t you? You realize that the probabilities of finding new functional genes that way is practically nil, don’t you?

    So, how do you explain the findings in that article?

    Those are very good examples of design.

  32. 32
    Joe says:

    Evolve- why do you just take Miller’s word for it? Also Miller is totally wrong because the alleged fusion occurred in the HUMAN lineage and didn’t have anythiung to do with any alleged common ancestry with chimps.

  33. 33
    bornagain77 says:

    Here is a good summary of why the chromosome 2 argument does not wash – 2012
    http://www.uncommondescent.com.....ent-431951

    It’s Cherry Picking Season – July 24, 2012
    Excerpt (Guy walks into a bar and thinks he is a chimp): I try to outline all the functions of telomeric repeats, but my friend tells me that I am getting off the subject.
    He wants to me to focus on the ITSs, the tracks of the hexamer TTAGGG that reside within chromosome arms or around the centromere, not at the ends. I tell him that I was just coming to that topic. The story, you see, is that in the lineage leading up (or down, I forget which) to chimps and humans, a fusion of chromosome ends occurred — two telomeres became stuck together, the DNA was stitched together, and now we find the remnants of this event on the inside of chromosomes. And to be fair, I concede at this point that the 2q13 ITS site shared by chimps and humans can be considered a synapomorphy, a five-dollar cladistic term meaning a genetic marker that the two species share. As this is said, it is apparent that the countenance of my acquaintance lightens a bit only to darken a second later. For I follow up by saying that of all the known ITSs, and there are many in the genomes of chimps and humans, as well as mice and rats and cows…, the 2q13 ITS is the only one that can be associated with an evolutionary breakpoint or fusion. The other ITSs, I hasten to add, do not square up with chromosomal breakpoints in primates (Farré M, Ponsà M, Bosch M. 2009, “Interstitial telomeric sequences (ITSs) are not located at the exact evolutionary breakpoints in primates,” Cytogenetic and Genome Research 124(2): 128-131.). In brief, to hone in on the 2q13 ITS as being typical of what we see in the human and chimp genomes seems almost like cherry-picking data. Most are not DNA scars in the way they have been portrayed.
    http://www.evolutionnews.org/2.....62491.html

    The chromosome 2 fusion model of human evolution—part 1: re-evaluating the evidence – Jerry Bergman and Jeffrey Tomkins
    Conclusion: The purportedly overwhelming DNA evidence for a fusion event involving two primate chromosomes to form human chromosome 2 does not exist, even without the aid of new analyses. In this report, our review of only the reported data by evolutionary scientists shows that the sequence features encompassing the purported chromosome-2 fusion site are far too ambiguous to infer a fusion event. In addition to a lack of DNA sequence data for a head-to-head chromosomal fusion, there also exists a decided paucity of data to indicate a cryptic centromere. In a companion paper (part 2) to this, we report the results of additional data analyses using a variety of bioinformatic tools and publicly available DNA sequence resources that further refute the hypothetical chromosome fusion model.
    http://creation.com/chromosome-2-fusion-1

    What I Said about Chromosomal Fusion and Why I Said It – David Klinghoffer – July 23, 2012
    Excerpt: [T]he evidence for chromosomal fusion isn’t nearly as clear-cut as evolutionists like [Kenneth] Miller claim.
    Telomeric DNA at the ends of our chromosomes normally consists of thousands of repeats of the 6-base-pair sequence TTAGGG. But the alleged fusion point in human chromosome 2 contains far less telomeric DNA than it should if two chromosome were fused end-to-end: As evolutionary biologist Daniel Fairbanks admits, the location only has 158 repeats, and only “44 are perfect copies” of the sequence.46
    Additionally, a paper in Genome Research found that the alleged telomeric sequences we do have are “degenerated significantly” and “highly diverged from the prototypic telomeric repeats.” The paper is surprised at this finding, because the fusion event supposedly happened recently — much too recent for such dramatic divergence of sequence. Thus the paper asks: “If the fusion occurred within the telomeric repeat arrays less than ?6 mya [million years ago], why are the arrays at the fusion site so degenerate?”47 The conclusion is this: If two chromosomes were fused end-to-end in humans, then a huge amount of alleged telomeric DNA is missing or garbled.
    Finally, the presence of telomeric DNA within a mammalian chromosome isn’t highly unusual, and does not necessarily indicate some ancient point of fusion of two chromosomes. Evolutionary biologist Richard Sternberg points out that interstitial telomeric sequences (ITSs) are commonly found throughout mammalian genomes, but the telomeric sequences within human chromosome 2 are cherry-picked by evolutionists and cited as evidence for a fusion event….
    http://www.evolutionnews.org/2.....62451.html

    More notes:

    https://docs.google.com/document/d/1enllGchcY4Thz0xWFG8Rj8Y0bddOcBdIzKeoY1XxSqs/edit

  34. 34
    Roy says:

    Now this is a particularly interesting accusation for you, a Darwinist, to make, since Darwinists are notorious for smuggling in information into their evolutionary algorithms (i.e. Dawkins’ targeted Weasel phrase).

    “Smuggling”?

    Dawkins stated up-front exactly how the program worked and where the target string came from. If you think that’s smuggling, you’re deluded.

    Roy

  35. 35
    Evolve says:

    VJTorley,

    ///I think it’s very easy to explain that fact: all one needs to posit is three successive acts of tweaking, over the course of geological time: a first act, which led to the divergence of African great apes from orangutans; a second act, which caused the African great apes to split into two lineages (the line leading to gorillas and the line leading to humans, chimps and bonobos); and finally, a third act, which led humans to split off from the ancestors of chimps and bonobos.///

    This is a classic creationist strategy of claiming God did it in such a way that one can’t distinguish his mode of creation from evolution.

    The problem you have with this scenario is that God becomes redundant & unnecessary to explain the data, unless you can provide evidence that he existed during the time and interfered with earth’s creatures in the manner you claim. You’re also placing constraints on your God by saying he operated on a minimum effort principle.

    By the way, can you name those genes Mr. God introduced at every point and how they impart the unique characters of each ape species? They shouldn’t exhibit the mutation rate we observe universally. It can be tested.

  36. 36
    bornagain77 says:

    Roy, thanks for the usual Darwinian ad hominem. Must be tough for you to put up with people so much less intellectual than you are! 🙂 But if memory serves me correctly, Dawkins was very ‘unforthright’ with his program. In fact, Dawkins Weasel program was mysteriously lost (perhaps his dog ate it) upon request by Dembski and others to see it:

    Dawkins’ WEASEL: Proximity Search With or Without Locking? – 2009
    http://www.uncommondescent.com.....t-locking/

    Provide the Code for Dawkins’ WEASEL Program
    http://www.uncommondescent.com.....l-program/

  37. 37
    Evolve says:

    Joe @ 32

    ///Evolve- why do you just take Miller’s word for it? ///

    You don’t have to take anybody’s word for it. You can check the sequence database and find out for yourself.

    ///Also Miller is totally wrong because the alleged fusion occurred in the HUMAN lineage and didn’t have anythiung to do with any alleged common ancestry with chimps.///

    Oh yeah, that’s why we see chromosome banding, gene arrangement & sequence alignment on human chromosome two to correspond with the respective ones on chimp, gorilla & orangutan chromosomes.

  38. 38
    bornagain77 says:

    So evolve, since no one has ever seen evolutionary processes generate a single gene or protein, and yet God is unthinkable to your atheistic preferences of how things out to be, then materialistic processes must have done it in spite of the fact that you have no evidence that material processes can generate functional information? Ever here of ‘begging the question’?

    1. Consciousness either preceded all of material reality or is a ‘epi-phenomena’ of material reality.
    2. If consciousness is a ‘epi-phenomena’ of material reality then consciousness will be found to have no special position within material reality. Whereas conversely, if consciousness precedes material reality then consciousness will be found to have a special position within material reality.
    3. Consciousness is found to have a special, even central, position within material reality.
    4. Therefore, consciousness is found to precede material reality.

    Four intersecting lines of experimental evidence from quantum mechanics that shows that consciousness precedes material reality (Wigner’s Quantum Symmetries, Wheeler’s Delayed Choice, Leggett’s Inequalities, Quantum Zeno effect):
    https://docs.google.com/document/d/1G_Fi50ljF5w_XyJHfmSIZsOcPFhgoAZ3PRc_ktY8cFo/edit

    Colossians 1:17
    And he is before all things, and by him all things consist.

  39. 39
    bornagain77 says:

    evolve, you claim that genomic similarity is overwhelming

    Oh yeah, that’s why we see chromosome banding, gene arrangement & sequence alignment on human chromosome two to correspond with the respective ones on chimp, gorilla & orangutan chromosomes.

    Yet you forgot to mention:

    “Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic archetecture outside the protein coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things organized and used are vastly different between a chimpanzee and a human being in their genomes.”
    Raymond Bohlin (per Richard Sternberg) – 9:29 minute mark of video
    http://www.metacafe.com/watch/8593991/

  40. 40
    gpuccio says:

    BA:

    I checked the article you quoted at #26, and the original paper just published in Nature. Simply wonderful, as usual you are the best at finding the most interesting stuff.

    The tons of detailed information that are accumulating thanks to new technologies (like RNA-seq) are amazing, and their meaning is just starting to appear. Poor neo-darwinists!

    I would like to cite here just one of the most surprising results in the paper:

    Most transcriptional complexity in Drosophila occurs in tissues of the nervous system, and particularly in the functionally differentiating central and peripheral nervous systems. A subset of ultra-complex genes encodes more than half of detected transcript isoforms and these are dramatically enriched for RNA editing events and 3′ UTR extensions, both phenomena largely specific to the nervous system. Our study indicates that the total information output of an animal transcriptome may be heavily weighted by the needs of the developing nervous system.

    And:

    majority of transcriptome complexity is attributable to forty-seven genes that have the capacity to encode > 1,000 transcript isoforms each (Supplementary Table 3), and account for 50% of all transcripts (Fig. 3a). Furthermore, 27% of transcripts encoded by these genes were detected exclusively in samples enriched for neuronal tissue, and another 56% only in the embryo (83% total).

    Do you realize? And all that in drosophila! What would they find in humans, I wonder?

    I suppose that the ear of “junk DNA” junk is definitely over. Transcriptomics and other bottom up approaches have just started to amaze us. Transcription regulation is what really counts, and the levels of functional complexity will increase of so many orders of magnitude in the next few years that it will be really interesting to see how neo-darwinists cope with that (OK, I know, they are very good at that, they will not disappoint us!).

  41. 41
    Roy says:

    ba77:

    Roy, thanks for the usual Darwinian ad hominem.

    Wrong as usual.

    Concluding that your claims are ridiculous because you are deluded would have been an ad hominem. Concluding that you are deluded because your claims are ridiculous is not.

    Roy

  42. 42
    Timmy says:

    gpuccio #18:

    I accept, at present, common descent as the best available explanation for the majority of empirical observations. I agree with VJ, and Behe, and others, on that point.

    I mean in this in the most honest way: what would you (or others who share your view) consider to be the best two or three or four observations that are best explained by the common descent?

    My problem is, how can any level of similarity be argued to imply common descent unless all the differences between the two organisms lie within the limits of evolution (i.e., no differences in integrated systems, etc.)?

    I mean, what is the explanatory value in positing common descent if one has already invoked the designer? Surely, for example, the differences between chimps and humans far exceed the limits of evolution.

  43. 43
    niwrad says:

    Larry Moran’s “proof” of the ape-like-ancestor to human evolution is based on a series of unsupported claims:

    (1) actually there is no proof that DNA is the unique cause of the formation of a certain species. It is likely that many other factors play a role.

    (2) also if #1 is ok, 98.6% genomic identity between chimp and human (= 22.4 million DNA bases) is highly debatable, because genomic comparison can be done in many different ways and depends on many presuppositions.

    (3) also if #1,2 are ok, 130 mutations fixed in the human population in each generation is another highly debatable issue.

    (4) also if #1,2,3 are ok, no one can prove that such 130 mutations fixed are exactly those necessary to the transformation.

    (5) also if #1,2,3,4 are ok, no one has proved that natural selection passed along those mutations. Lab experiments show that natural selection passes along a beneficial mutation when it has at least a 10% fitness advantage.

    (6) also if #1,2,3,4,5 are ok, it is again highly debatable and unproved that chimps and humans diverged five million years ago, based on fossils. Fossils tell nothing about the deep differences between man and apes. For example, can a fossil prove a difference in intellect?

    As a consequence Moran’s claim about human evolution from ape-like-ancestor based on the very simple computation “130 x 185,200 = 22.4 million mutations” is ridiculous and gives a good idea of the lack of reliability of Darwinian biology.

  44. 44
    vjtorley says:

    Hi Timmy,

    Excellent question. You asked:

    My problem is, how can any level of similarity be argued to imply common descent unless all the differences between the two organisms lie within the limits of evolution (i.e., no differences in integrated systems, etc.)?

    To answer your question, I’d like to return to a remark made by Todd Wood in his 2006 article:

    The question is not how similarity arose but why this particular pattern of similarity arose. To say that God could have created the pattern is merely ad hoc. The specific similarity we observe between humans and chimpanzees is not therefore evidence merely of their common ancestry but of their close relationship.

    Notice that the foregoing argument deliberately leaves the question of evolutionary mechanisms to one side. It implicitly assumes the existence of an agent with an unlimited capacity to surmount the differences that exist between any two species. If we make that assumption, then we can indeed view the pattern of similarity between humans and chimps as evidence for common ancestry.

    The second point I’d like to make is that the assumption of common ancestry enables us to make some powerful predictions regarding future similarities that we’ll discover between humans and chimps. For instance, it predicts that we’ll find more and more shared pseudogenes. And as Todd Wood writes, “it is difficult to explain why pseudogenes with the exact same substitutions or deletions would be shared between species that did not share a common ancestor.” Notice again that he is making a “why” argument, which implicitly presupposes that “how” is not a problem. This kind of argumentation is perfectly legitimate, if one assumes the existence of a Designer, as I do (and as Todd Wood does).

    But you’ve hit on a very powerful argumentative point, Timmy. If you are trying to put forward an unguided mechanism as the explanation for the variety of life-forms we see on Earth today, then it is not enough to account for levels of similarity, or even to make predictions regarding future discoveries of shared similarities. You have to specify a mechanism that is adequate to account for the differences between humans and chimps. Until you can do that, then any rhetorical theological arguments you put forward, asking why a Creator would make animals with these odd similarities, really cut no ice: your hypothesis is powerless.

    Darwin’s contemporaries should have realized this. Instead, they wilted under the rhetorical force of his book and turned into nervous Nellies, asking each other, “What if he’s right after all? What if natural selection can generate new species?” without demanding proof that it could. In such a frame of mind, they let Darwin’s “Why would God have done it that way?” argument bamboozle them. For the first thing a hypothesis has to do is explain the “how” questions, not the “why” questions. Darwinism couldn’t do that, but Darwin’s argumentative brilliance lay in the fact that he managed to divert his contemporaries’ attention away from that key point.

  45. 45
    gpuccio says:

    Timmy:

    For me, the best evidence of common descent is molecular: the pattern of homologies and differences in proteins which have similar function and structure in more or less distant species. The differences are usually proportional to the distance (I will not enter here in the discussion about trees of life. Let’s say that the same protein in bacteria is usually much more different, at the sequence level, if compared to the human form than, say, the same protein in c. elegans or the same protein in a fish). The best explanation for that, IMO, is that neutral mutations in time change the sequence, while the structure and function are mostly well conserved. That effect is rather consistent, and can be verified by anybody by blasting old proteins which are present in all animals. Frankly, I find it difficult to explain those facts completely by functional constraints (the common design explanation).

    On the other hand, I agree that the inconsistencies about trees of life, and especially the recent ones originated by the use of miRNAs, are good arguments against CD, or at least against the conventional models of CD.

    I would really leave the problem open. I don’t think that the facts available can give a final answer to that point. Let’s be patient, and pursue good scientific explanations with an open mind.

  46. 46
    gpuccio says:

    VJ:

    I very much agree with you on these points. I would also emphasize the important paper cited by BA, and which I briefly commented in #40. It is really amazing how a very small number of genes in drosophila can be so overwhelmingly complex at transcription level, and be so strongly associated with the development of the nervous system. That can suggest that all the traditional arguments about “similarities” between humans and chimps (or any other couple of species) should be reevaluated in terms of transcription regulation rather than in terms of genomics, especially now that we have the tools to quantitatively explore transcription.

    After all, without any offense to the chimps (who are very good people), the human brain is really much more complex!

  47. 47
    vjtorley says:

    Hi Evolve,

    Just a quick note to say that I’m looking into your claims at the moment. I’ll get back to you as soon as I can. Cheers.

  48. 48
    Joe says:

    Evolve punts:

    Also Miller is totally wrong because the alleged fusion occurred in the HUMAN lineage and didn’t have anything to do with any alleged common ancestry with chimps.

    Oh yeah, that’s why we see chromosome banding, gene arrangement & sequence alignment on human chromosome two to correspond with the respective ones on chimp, gorilla & orangutan chromosomes.

    Non-sequitur. BTW chromosome banding is the result of the technique used.

  49. 49
    Joe says:

    evolve:

    This is a classic creationist strategy of claiming God did it in such a way that one can’t distinguish his mode of creation from evolution.

    How can we test the claim that blind watchmaker evolution is capable of doing it?

  50. 50
    scordova says:

    Thanks for the mathematical exposition. I think I can understand the logic now; I wish Professor Moran had explained it in the posts I cited

    Sorry to be cynical Dr. Torley, but obfuscation rather than education of the readers helps them make their case. I had to say something because that’s what I was seeing happen.

    Field measured mutation rates are too expensive to do really well. But to the extent they are done, they agree with those arguing for a literal flood and Ark (not necessarily YEC, since the flood account is compatible with OEC).

    http://www.examiner.com/articl.....-years-old

    The article mentions both human mitochondrial eve and cattle mitochondrial eve. 🙂

  51. 51
    Evolve says:

    Torley @ 44

    ///If you are trying to put forward an unguided mechanism as the explanation for the variety of life-forms we see on Earth today, then it is not enough to account for levels of similarity… You have to specify a mechanism that is adequate to account for the differences between humans and chimps.///

    The mechanism has been specified and its predictions have been validated. The observed number of nucleotide substitutions between humans & chimps matches the rate of mutation as explained by Larry Moran. What more do you want? How is your proposed mechanism of a totally imaginary designer better?
    You can twist any explanation offered in support of evolution to fit your designer, as you demonstrated above in your ridiculous account of ape ancestry! When will you realize that such an approach won’t hold water, Mr. Torley?

    ///The second point I’d like to make is that the assumption of common ancestry… This kind of argumentation is perfectly legitimate, if one assumes the existence of a Designer, as I do.///

    Common ancestry is NOT an assumption and you cannot talk about it in the same vein as assuming an imaginary designer. Common ancestry is the best explanation of the data; because it is not just about shared similarities and differences – those similarities and differences exhibit a pattern of NESTED HIERARCHY.

    Closely related organisms form a taxonomic group with features unique to that group, but which is nested within a larger group of organisms that are linked by a broader range of unique features. Traits specific to one group are not found outside of it.

    In fact what we see is a twin nested hierarchy – one in anatomical traits and another in the DNA (not just in genes, but in the entire genome including non-coding and junk DNA).

    Why are feathers found only in birds? And why do we recover fossil feathered dinosaurs? Why not feathered mammals? What does that tell you? Why is hair found only in mammals and not in reptiles or birds?
    Why do whales & dolphins have rudimentary pelves and whiskers although they resemble fish? And why have we dug up fossil specimens with intermediate features between land mammals and fully aquatic whales?

    Humans have 3 tiny bones inside their middle ear, a feature found in all other mammals – extinct & extant, but not in other animal groups. Why?
    In reptiles, two of these bones are part of the jaw. And we’ve got fossils showing intermediate stages of the transition between these two states. How do you explain this from a design standpoint?

    Your explanation must account for all these observations. A word salad about “whys” and “hows” will not work.

    The nested hierarchy pattern exhibited by living things is damning for the idea of a designer. Human-designed objects share similarities but they do not form nested hierarchies. eg: automobiles. End of Story.

  52. 52
    Evolve says:

    Joe @ 49

    ///Non-sequitur. BTW chromosome banding is the result of the technique used.///

    Then why don’t we find the same banding in a dog chromosome, if it is a result of the technique? Between, it’s not just similar banding, but also similar gene arrangement and DNA sequence – all in a nested hierarchy pattern. The evidence is pretty much conclusive (unless you want to keep on denying everything of course).

  53. 53
    Evolve says:

    Joe,

    ///How can we test the claim that blind watchmaker evolution is capable of doing it?///

    Evolution IS an observed fact happening around you constantly. Living organisms change one step at a time every single generation. What stops small changes from accumulating over vast time periods to result in a big change? Nothing.

    We see this in the DNA and in the fossil record in the expected pattern.

    Otherwise, how do you explain a series of transitional fossils between a land animal and a whale, each progressively more suited to an aquatic lifestyle? If the designer wanted to create a whale, why bother doing it bit by bit incrementally? Oh yeah, I know, that’s how the designer wanted to do it! Great!

  54. 54
    HD says:

    Evolve,

    I don’t understand the real issue. Mr. Torley accepts common ancestory. That means, he also accepts macro-evolution and all the evolutionary and transitional steps in between. (After all, how do you get from a common ancestor to divergent chimps and humans UNLESS there is transitions in between).

    So are you just arguing over details, or are you arguing that he is simply wrong to believe in a god?

    thanks

  55. 55
    Joe says:

    Evolve-

    Intelligent Design is not anti-evolution. How can we tell if the evolution we observed is blind watchmaker or not?

    As for the alleged whale evolution- how many transitions did it take? How many mutations? How can we test the claim that blind watchmaker evolution didit?

    Genetic algorithms show us the power of guided evolution. No one can even model unguided evolution. You lose.

  56. 56
    Joe says:

    Evolve,

    Similar genomes can be explained by both a common design and convergence. And seeing that the bulk of the genome is for running daily things as opposed to building the organism, I would expect the bulk of most genomes to be similar, especially given a common design.

    And gradual evolution would not produced nested hierarchies. Transitional forms, by their very existence, is evidence against objective nested hierarchies. And gradual evolution predicts many transitional forms. So please stop using terms that you obviously don’t understand.

  57. 57
    Joe says:

    Nested hierarchies are purely a manmade construct and do not reflect anything but our attempt at cleverness. Linnean taxonomy was based on a common design that used defining characteristics as the criteria for sets and levels.

    Also the US Army is a nested hierarchy and it doesn’t have anything to do with common descent.

    Gradual evolution would predict many transitional forms which have a mix of defining characteristics and that would create a smooth blending leaving the sets ill-defined, without any distinct boundaries. Nested hierarchies require distinct boundaries and you can’t have that with gradual evolution.

  58. 58
    vjtorley says:

    Hi Evolve:

    Back again. So who’s right: Tomkins or Miller? Short answer: Tomkins. Here’s a short reply from an academic who teaches microbiology:

    ENCODE is right.

    Tomkins pulls the data from ENCODE and there is clearly a gene transcribed across the fusion event. The gene is rather larger than the 1500 bp that Miller quotes. The gene is a helicase (if I remember correctly) expressed in various tissues throughout development. If you read Tomkins’ paper, he demonstrates where the supposed telomere ends are located, where additional centromeres are supposedly located, and how the region is transcriptionally active (a hallmark associated with non-telomeric DNA).

  59. 59
    vjtorley says:

    Hi Evolve,

    Re orphan genes, you wrote:

    ..there’s no escaping the evidence. The Science paper did RNA-seq on the testis transcriptome of few D. melanogaster strains and identified several newly-transcribed genes which were absent from the D. melanogaster reference sequence. A sequence alignment showed that these new genes corresponded to intergenic regions in the D. melanogaster reference sequence and orthologous regions of closely related species such as D. simulans & D. yakuba. This clearly shows that new genes can arise by mutations in previously non-expressed DNA and it contributes to speciation.

    Here’s a reply from an informed source:

    From what I can read, Evolve fails to recognize the human error and computer error associated with annotating genomes. Computer programs are written to identify certain features that the molecular biologists look for when identifying where to find genes. Any molecular biologist with sufficient training recognizes that those algorithms are not 100% perfect. If RNAseq data shows genes were transcribed, there is no denying the transcript–only denying the bioinformatics. Unfortunately, we often only find what we’re looking for.

    Hope that helps. Cheers, and thanks very much for your participation in this discussion.

  60. 60
    vjtorley says:

    Hi Evolve,

    Re the reports you referenced on orphan genes, here’s a comment from an academic source:

    When you read this it sounds so compelling. “Oh my gosh there are transcribed genes in some flies that are absent from the reference sequence?”

    No. They are ancestral genes that have been mutated and lost in a proportion of the population that includes where they got the reference sequence from. It is the complete opposite of what they are claiming.

  61. 61
    bornagain77 says:

    Thanks Dr. Torley for taking time to clear that up

  62. 62
    bornagain77 says:

    Follow-Up: Refuting Ken Miller on Chromosome 2 – 2012 – video
    http://www.youtube.com/watch?v=YJikA1gH7CY

  63. 63
    Timmy says:

    I appreciate the replies.

    vjtorley #44:

    As far as I can tell, all similarity necessarily implies (similarity in information, of course) is copying. But it does not necessarily tell us anything about the copying mechanism. Common ancestry is such a mechanism, so is plagiarism, so is the use of a code library. So my question is, what details of the similarity could lead us to infer a particular mechanism? Obviously certain conditions allow us to infer all three of the above mechanisms. However common ancestry between different species is a bit harder. What is it about substitutions/deletions in pseduogenes that infer common ancestry over and above the designer simply reusing his code? (Sorry if this is obvious but I can’t say it’s my field!)

    Second point: once everyone is on the same page regarding the limits of evolution and the fact of design, the theology (“why did God do it that way?”) becomes very interesting. From a human perspective, for example, it would make a lot of sense to engineer an organism through trial and error (common descent): let it live for a while, observe what happens, make changes based on mission objectives, and so on. However, presumably God hasn’t got these limits, so what would common descent tell us about God? Difficult to say.

    gpuccio #45:

    Thanks for the clear answer. I can’t say I’m especially bothered by common descent, I just want to understand the circumstances under which it can be inferred as a copying mechanism vs. some other copying mechanism (since I do not have enough background knowledge of genetics one way other other).

    So if I read you right, (and I am going to jump to a conclusion here), you are reflecting some sort of punctuated saltation, where species A lives for some length of time, accumulating evolutionary changes/errors to its code, and then kaboom!, the designer injects new code into some sub-population of species A, creating species B, which then lives for a while and then species C is created and so on and so forth. So when we compare the code between species A and Z and species C and Z, etc. we observe accumulation deltas that reflect the inherited relationship?

    Or, if I am totally off base, what is it about the type of patterns you refer to that might preclude common design? That’s really what I want to get at. How are we to judge between copying mechanisms? (This is pretty much a repeat of what I wrote to Dr. Torley.)

    Evolve #51 writes:

    What more do you want? How is your proposed mechanism of a totally imaginary designer better

    What I want is a mechanism actually capable of engineering the new and improved systems found in humans. Is that too much to ask?

  64. 64
    scordova says:

    Dr. Torley,

    It’s deep in the weeds, but one potentially very devastating argument that hasn’t made the forefront, but should eventually is polyconstrained DNA. It was featured in the Cornell conference.

    Personally it casts serious doubt on neutral evolution or Darwinian evolution. Here’s an easy intro:

    http://bevets.com/equotess.htm

  65. 65

    I’d like to follow up Rob and Sal’s mathematical analysis of fixation of mutations (this is also relevant to our previous discussion of orphan sequences).

    R. A. Fisher did pioneering work in the theoretical understanding of the effects of various kinds of mutations under various types of selection pressures and under conditions that would favor drift (the latter were refined by Sewall Wright). According to their analyses, a mutation (defined as any change in the genetics of an organism) can have one of three mutually exclusive phenotypic effects and one of three mutually exclusive outcomes as the result of differential survival and reproduction.

    A mutation can be expressed as:

    • dominant (masking a recessive alternative),

    • recessive (masked by a dominant alternative), or
    • intermediate (expressed as a blend with the expression of its alternative).

    The phenotypic expression of a mutation can be:

    • beneficial (increasing in frequency as a result of increased relative survival and reproduction of its carrier),

    • deleterious (decreasing in frequency as a result of decreased relative survival and reproduction of its carrier), or
    • neutral (fluctuating randomly in frequency as a result of random relative survival and reproduction of its carrier).

    It is essential to realize here that there is no necessary relationship between the inheritance pattern of a mutation and its effect on survival and reproduction: a dominant mutation can be beneficial, deleterious, or neutral, as can a recessive or intermediate mutation.

    To analyze the effects of the interactions between these conditions, let us assume that mutations arise singly, randomly, and at low frequency in a population (i.e. not simultaneously among many individuals, not in any particular “direction” vis-à-vis differential survival and reproduction, and only very rarely).

    Finally, for the purposes of comparative analysis, a population can be relatively large or small.

    Under the various combinations of these conditions (all of the following are verbal descriptions of what are actually mathematical relationships):

    • A mutation that is dominant and beneficial may increase in frequency in a population, as its carrier will express a genetic tendency to have a phenotype that results in increased survival and reproduction. However, since its frequency is very low (i.e. mathematically, one over the number of individuals in the population), it is likely that it will disappear as the result of random chance (i.e. it will be eliminated as the result of drift), since the probability of a mutation going to fixation is mathematically the same as its frequency in the population.

    Ergo, beneficial dominant mutations are likely to flicker in and out of existence in all except relatively small populations.

    • In relatively small populations, individuals with dominant beneficial mutations are more likely to increase in frequency, as they constitute a higher relative frequency of a small population than they would in a larger one.

    • A mutation that is dominant and deleterious will almost immediately disappear, as its carrier will express a genetic tendency to have a phenotype that results in decreased survival and reproduction. Again, since its frequency is very low, it is also likely that it will disappear as the result of drift.

    • In relatively small populations, individuals with dominant deleterious mutations are more likely to decrease in frequency, as they constitute a higher relative frequency of a small population than they would in a larger one.

    Ergo, deleterious dominant mutations are likely to disappear in virtually all populations, regardless of size.

    • A mutation that is recessive and beneficial will not initially increase in frequency in a population, as its carrier will not express the genetic tendency to have a phenotype that results in increased survival and reproduction (it will be masked by the dominant alternative). Again, since its frequency is very low (i.e. one over the number of individuals in the population), it is likely that it will disappear as the result of drift.

    Ergo, beneficial recessive mutations are just as likely to flicker in and out of existence as dominant ones in all except relatively small populations.

    • However, in relatively small populations, individuals with recessive beneficial mutations will show a “threshold effect”, as they are relatively more likely to combine in homozygotes and therefore rapidly increase in frequency, again because they constitute a higher relative frequency of a small population than they would in a larger one.

    • A mutation that is recessive and deleterious will not initially decrease in frequency in a population, as its carrier will not express the genetic tendency to have a phenotype that has an decreased probability of survival and reproduction, as it will be masked by the dominant beneficial alternative. Again, since its frequency is very low, it is very likely that it will disappear as the result of drift.

    • However, if by chance its frequency increases (for example, in a relatively small population), it will eventually reach a threshold value at which homozygous recessive individuals will phenotypically express the mutation. The result would be a concomitant decrease in the frequency of the mutation as the result of decreased survival and reproduction.

    Ergo, deleterious recessive mutations are likely to disappear in virtually all populations, but especially in relatively small populations in which they will be more often expressed and eliminated in homozygotes.

    • A mutation that is intermediate (i.e. expressed equally with its genetic alternatives) will essentially perform the same way a dominant mutation will, as it will be expressed in those individuals that carry it.

    Ergo, intermediate mutations will also tend to flicker in and out of existence in all except relatively small populations.

    • In small populations, intermediate mutations have generally the same effects as dominant ones: if beneficial they will rapidly increase, if deleterious they will rapidly disappear.

    Note the asymmetries in outcomes, especially with respect to population size:

    • Beneficial and intermediate mutations may either increase or decrease in frequency, depending on population size.

    • Beneficial and intermediate mutations are more likely to increase in frequency if the population size is relatively small, as the probability of accidental removal as the result of drift decreases in smaller populations.

    • Deleterious mutations are more likely to decrease in frequency in any size population, but especially if they are dominant or if the population is relatively small.

    Fisher then analyzed what would happen if the environment changed in such a way as to make a formerly beneficial trait deleterious:

    • If it were dominant or intermediate it would decrease in frequency, especially if the population were relatively small.

    • If it were recessive it would also decrease in frequency, especially if the population were relatively small.

    This would mean that the alternative form (i.e. the newly beneficial alternative) would increase in frequency, either monotonically or after reaching a “threshold of expression”, especially in relatively small populations.

    • The result would be the elimination of the formerly beneficial (and now deleterious) form and the fixation of the alternative form.

    • If a new mutation were then to occur, it would follow the same patterns analyzed above.

    One more factor needs to be included here: random mutations are more likely to be either deleterious or neutral than beneficial. This is because of what could be called the “Swiss watch effect”:

    • If you randomly alter one of the parts of a Swiss watch (say, by poking in ice pick into its innards), the more likely outcome is a decline in its function.

    • By the same logic, the simpler and more “fine-tuned” (i.e. tightly functionally interconnected) the watch, the more likely a random change will have a deleterious effect on its function.

    • Alternatively, the more redundant the mechanisms in the watch and the less “fine tuned” they are, the less deleterious a random change will be, compared with a simpler, more “fine-tuned” mechanism.

    The net effect of combining all of these outcomes is:

    • Beneficial mutations, while rare, will increase in frequency in populations, especially dominant mutations in relatively small populations.

    • Deleterious mutations, regardless of rarity, will decrease in frequency in populations, especially relatively small ones.

    Since these relationships were first proposed in the 1930s, they have been exhaustively tested, in both the field and laboratory. The outcome of such tests has generally upheld the predictions, with some interesting variations:

    • Some single-gene traits that are deleterious when homozygous are apparently beneficial when heterozygous (sickle cell anemia is the best-known example)

    • More traits have turned out to be neutral than predicted by the original version of the theory

    • Population size has a greater effect on outcomes than predicted by the original version of the theory; specifically, drift has turned out to be more important that the original theory predicted.

    One final note: “beneficial” can be translated as “functional” in all of the foregoing. Indeed, “functional” should be translated as “resulting in increased relatively survival and reproduction” in general.

  66. 66
    vjtorley says:

    Hi Allen MacNeill,

    Thanks very much for that interesting and illuminating exposition. Just one question: you and other commenters on this thread have asserted that “the probability of a mutation going to fixation is mathematically the same as its frequency in the population.” Why is this so? (It might sound obvious to you, but I’m afraid it isn’t to me.)

  67. 67
    vjtorley says:

    Here’s a question for the biologists. Can anyone find a single example of authentic telomere to telomere fusion?

  68. 68
    scordova says:

    VJ,

    Why is this so? (It might sound obvious to you, but I’m afraid it isn’t to me.)

    For a simple illustration, I’ll have to bend the rules just a bit so you can see.

    Let’s just have a population of 4 individuals, and we’ll just look at a particular nucleotide position. Each individual has a different “mutant” for the same nucleotide position. I describe the initial generation:

    Generation 0

    Individual #1: A
    Individual #2: C
    Individual #3: T
    Individual #4: G

    The mutant’s “compete” for primacy and at the end one of them has a monopoly on that nucleotide position.

    Now there are only 4 possible scenarios after infinite time (aka Generation infinity) since we’re almost guaranteed that one will go to fixation, we just don’t know which mutant prevails. I list the 4 possible outcomes:

    Generation Infinity

    Individual #1: A
    Individual #2: A
    Individual #3: A
    Individual #4: A

    or

    Individual #1: C
    Individual #2: C
    Individual #3: C
    Individual #4: C

    or

    Individual #1: T
    Individual #2: T
    Individual #3: T
    Individual #4: T

    or

    Individual #1: G
    Individual #2: G
    Individual #3: G
    Individual #4: G

    Those cover all the possible outcomes.

    We can see the probability of fixation of A is 1/4, C is 1/4, T is 1/4, G is 1/4. Thus the fixation probability is equal to the initial density of a particular mutant.

    With a little imagination you can see this extrapolate to 10,000 individuals and whatever proportion of the mutant there is. You just have to be clever in relabeling things.

  69. 69
    gpuccio says:

    Timmy:

    I appreciate your comments very much. I will try to answer.

    And the answer is simple. As you say, a copying mechanism is the best explanation for the similarities and differences we observe in the same functional protein across time. But, if I understand you well, you are suggesting that the copying does not happen in the “hardware” (the existing living beings), but elsewhere (the “software” is copied). Have I understood you well?

    So, let’s say that a designer has a repository of the software he used to build species A, then after some time he decides to build a new species, B, and he starts from his stored software for species A, modifies it with the new implementations, and then build species B. Is that the idea? That would be common design, but not from scratch. The solutions already developed would be reused.

    OK, that’s fine for me, but I ask two things:

    a) Why should we believe that the designer has some other non physical repository (possible, but we obviously have no direct evidence of that), when he reasonably can access the copies that are already around to implement the new functions? That would be, instead, common descent (but, obviously, with engineered modifications).

    b) What would be the observed difference between the two scenarios? It’s simple. In the second scenario (common descent) neutral modifications which happened in the time of existence of species A “on the market”, and did not modify the function, would be retained in species B, while that would not happen in the common design scenario, even with reuse of the software from the original repository.

    Now, that’s exactly what we apparently observe, and in great abundance. We know that protein function is redundant: many different sequences can generate the same structure and function. And in homologous protein, let’s say in bacteria and humans, we often observe only 30-40% sequence homology (while the function is the same), while we can ususally observe 80-90% between mouse and humans, for example, and let’s say 60% between C. elegans and humans. That’s the general pattern, and frankly I don’t believe that it can be explained saying that each observed difference is due to functional differences, and that none of them is neutral. There are even the synonimous mutations (DNA mutations which code for the same aminoacid and therefore do not alter the protein sequence), which are neutral by definition (OK, OK, I know that it is not always true, but in general it is probably true), and follow the same pattern.

    I would like to know your opinion on that.

  70. 70
    gpuccio says:

    VJ:

    If I understand well your answer in post #60 (by your informed source) to Evolve’s post #24, I must say that I don’t agree with your source, and agree with Evolve (on the facts, not the interpretation of them).

    To explain the observations in the cited paper as genes lost in the majority of strains and of related species seems really an ad hoc explanation. I cannot accept it, unless your source has some objective facts in its support.

    Moreover, there is now rather ampple evidence that new functionl genes can arise, and have arisen, from non coding DNA segments in the course of natural history, and often through some transposon activity.

    Is that evidence for a neo darwinian mechanism? Absolutely not. Indeed, it is evidence against it, and for design. As I have tried to explain in my answer to Evolve in my post #31.

    So, why do you think that there is any problem in new functional genes arising from non coding segments? That’s exactly what a designer would do to implement new information. While a neo darwinian mechanism could never do that, because it should use only RV, without any help from NS.

  71. 71
    vjtorley says:

    Hi gpuccio,

    In answer to your question, the source whom I consulted for #60 above adds:

    Here is the clue: " newly-transcribed genes which were absent from the D. melanogaster reference sequence" [a quote from an article cited by Evolve in #24 – VJT].

    What do you suppose the D. melanogaster reference sequence is? If you thought it was a consensus sequence you would be wrong. If you thought it was the definitive sequence you would be wrong. If you thought it was a representative sequence you would still be wrong.

    The reference sequence is simply the first sequence that was obtained.

    I hope that makes sense to you. For my part, I have no idea what a reference sequence is.

    I can see your point in #70 that the explanation in #60 appears rather ad hoc.

    I was, however, interested in this remark if yours: “there is now rather ample evidence that new functional genes can arise, and have arisen, from non coding DNA segments in the course of natural history, and often through some transposon activity.” Can you recommend an article written for the layperson, summarizing this evidence?

    Looking at your comment in #31 above, I find much to agree with. I especially liked this paragraph, addressed to Evolve:

    So, you realize that the paper tells us nothing about the mechanism of mutation, don’t you? You realize that according to this scenario the new gene should have evolved by RV alone, without any help from NS, at least until the new gene is ready and functional, don’t you? You realize that an unexpressed segment of DNA cannot be selected for function, don’t you? You realize that the probabilities of finding new functional genes that way is practically nil, don’t you?

    Hear, hear!

    If I understand you rightly, you seem to believe that the Designer (God) periodically creates new functional genes and pops them in non-coding sections of our DNA, knowing (and presumably intending) that they’ll be expressed sooner or later. What’s more, you seem to think this creative process goes on continually, throughout the lifetime of a species (usually reckoned at 5 million years or so): it happens “in the course of natural history,” as you put it, and you maintain that it’s been verified to occur. Personally, I had been inclined to favor a model in which the Designer creates the 1,000 (or is it 100?) unique orphan genes that characterize a species, all up-front, at the moment when that species appears in the fossil record. That would make the creation of orphan genes a rare event. It would of course be even rarer if different species of organisms tend to appear (and die out) in waves, every few million years or so. I found that an appealing hypothesis: it is also compatible with a form of essentialism, too, as I argued in an earlier post in response to Professor Moran.

    But now look what happens if we use your model. Average lifetime of a species: 5,000,000 years. Average number of orphan genes that characterize that species and no other: 100 to 1,000. Frequency with which orphan genes appear in that species, assuming they’re created continually over time: once every 5,000 to 50,000 years. Number of species on the planet: around 10,000,000. If new species appear and disappear fairly independently of one another, then we should be seeing 200 to 2,000 creative acts per year by the Designer, continually.

    Now I’m not saying that can’t happen. But that does take a bit of getting used to. If you’re right, we should be able to observe God in the very act of creating, if we have enough scientists and enough cell microscopes. Fascinating!

  72. 72
    gpuccio says:

    VJ:

    You have perfectly understood my point.

    Regarding the examples of new genes coming out of non coding genes, especially by transposon activity, I have found many examples in the literature, many of them discussed here at UD in the past. Now I have not the references, so I quote just a couple. One is the RAG1 protein, which appears in fish and is one of the main components of the adaptive immune system. It is considered transposon derived. Another example is a human specific protein, probably important for nervous development, which had clearly recognizable homologies in primates, where it was never transcribed and translated, and was therefore pure non coding DNA. In humans, a very simple final mutation transformed it into an ORF, and therefore it wa translated and active (unfortunately, I don’t remember the reference).

    The drosophila paper is perfectly compatible with this scenario. Moreover, the new genes were absent not only from the melanogaster reference sequence (however accurate it may be), but also from other drosophila parent species, if I remember well.

    I do believe that the designer, or designers, is constantly and intelligently working. That would also explain why we are finding that many genes implied in complex regulations in higher species are often already present in earlier simpler forms of life, where their role is still an enigma.

    The emergence of a new species is certainly a special creative moment, but I think it could rely on previous preparatory work. Let’s call it “Punctuated Intelligent Design”. 🙂

    Fascinating? Yes, fascinating.

  73. 73
    Evolve says:

    VjTorley @ 59 & 60

    ///No. They are ancestral genes that have been mutated and lost in a proportion of the population that includes where they got the reference sequence from. It is the complete opposite of what they are claiming.///

    Wrong! Ancestral genes that have been mutated and lost in extant populations can be detected by phylogenetic methods. In the Science paper they find that the new genes are derived from ancestral intergenic unexpressed sequences.

    Here’s another paper reporting the origin of a new gene called Poldi from an intergenic region in mouse:

    http://www.sciencedirect.com/s.....2209014754

    The corresponding region is present in humans and rats, but do not produce a transcript.

    ///Evolve fails to recognize the human error and computer error associated with annotating genomes.///

    Lol, now you can start blaming the methodology! These are all standard procedures molecular biologists use.

    gpuccio @ 31 & 70

    ///So, you realize that the paper tells us nothing about the mechanism of mutation, don’t you? You realize that according to this scenario the new gene should have evolved by RV alone, without any help from NS, at least until the new gene is ready and functional, don’t you? You realize that an unexpressed segment of DNA cannot be selected for function, don’t you? You realize that the probabilities of finding new functional genes that way is practically nil, don’t you?

    Is that evidence for a neo darwinian mechanism? Absolutely not. Indeed, it is evidence against it, and for design. As I have tried to explain in my answer to Evolve in my post #31.///

    How is this evidence for design?
    New genes arise by mutations in intergenic sequences which allow it to be transcribed, spliced and expressed – nothing that we don’t understand already!
    Natural Selection is not the only process by which new mutations get fixed, you can get that by random genetic drift too. Another mechanism that we understand!

    In Fig. 3 of the Current Biology paper I posted above, they show changes in and around the new gene in a phylogenetic context. Guess what? The region is more similar in related mouse species and becomes more divergent in rats & humans as distance between species increases, exactly as evolution predicts.

    No magic is required here. Even if you explicitly want to invoke it, magic becomes superfluous since we can explain the data through already known natural mechanisms.

  74. 74
    Evolve says:

    Timmy @ 63

    ///What I want is a mechanism actually capable of engineering the new and improved systems found in humans. Is that too much to ask? ///

    I don’t get you. The well-understood mechanisms of mutation, natural selection, random genetic drift and neutral theory explain the evolution of all life that we know of, including humans. The predictions made by these theories have been tested and validated numerous times.

    If you think a magical designer is involved, then you’re more than welcome to topple evolutionary theory by elaborating how it better explains all the observed molecular, anatomical and fossil data. No one is stopping you from publishing your world-changing discovery in Science & Nature. Go ahead!

  75. 75
    vjtorley says:

    Hi Sal,

    Thanks very much for your clear exposition of the logic behind the statement that the probability of a mutation going to fixation is mathematically the same as its frequency in the population. I instantly realized what was wrong when I read this sentence:

    Now there are only 4 possible scenarios after infinite time (aka Generation infinity) since we’re almost guaranteed that one will go to fixation, we just don’t know which mutant prevails.

    1. This is a mathematical idealization. The phrase “after infinite time” has no real meaning, as there is no “after” infinity. Moreover, (n+infinity) is the same as infinity.

    2. In the real world, where the environment is in a state of continual upheaval and the assumption of constancy is never true, even for a short period, we are not guaranteed that one allele will eventually go to fixation.

    3. In a population where there are n individuals, each with its own distinct version of a given gene, we can reasonably assume that the ultimate triumph of individual A’s version is just as likely as the ultimate triumph of individual B’s version (especially if all versions are neutral). But it is far from clear to me that if individual A has version X and all other individuals have version Y, the ultimate triumph of individual A’s version is (1/n) as likely as the ultimate triumph of some other individual’s version (Y). For any number of a variety of reasons, A’s version might have a far greater disadvantage than that: it could be (1/n^2), for all we know. To assume that A has just as much chance as “any other individual” is begging the question, for individual A is not in a race with “any other individual,” but with every other individual. A’s odds of winning could be a lot longer than n:1.

    Maybe I’m just terribly thick. But even as an idealization (ignoring #2), it is far from clear to me that the outcome will be as described in the model case. And in the real world, where equilibrium is always being disturbed, that assertion seems doubly doubtful. Am I missing something?

    Thanks very much for your time and trouble by the way, Sal.

  76. 76
    Joe says:

    Evolve is conmfused. Evolutionism doesn’t explain “molecular, anatomical and fossil data”. Evolutionism can’t even explain eukaryotes, Evolve.

  77. 77
    Joe says:

    Evolve sez:

    The well-understood mechanisms of mutation, natural selection, random genetic drift and neutral theory explain the evolution of all life that we know of, including humans.

    That is the propaganda, anyway.

    The predictions made by these theories have been tested and validated numerous times.

    What predictions? Natural selection doesn’t make any predictions, drift doesn’t make any predictions and neutral theory doesn’t make any pr4edictions.

    You are just very gullible.

  78. 78
    vjtorley says:

    Hi Evolve,

    Thank you for your comment. I’d like to draw your attention to gpuccio’s remark, “You realize that an unexpressed segment of DNA cannot be selected for function, don’t you?”

    Pardon my ignorance of genetics, but I think the underlying idea that gpuccio is driving at is this. Very roughly, a gene can be defined as a piece of DNA coding for a protein (yes, I know that’s horribly simplistic). It does this by creating an RNA copy of the DNA, and the RNA copy has to get into a protein-making factory in the cell.

    As you’re aware, the research of Douglas Axe suggests that the probability of a given sequence of 100 amino acids actually being able to fold up into a protein that can carry out a biologically useful function is very low: about 1 in 10^77. (You would probably contest that figure, but humor me.) What’s more, as far as we can tell, all of these sequences are equiprobable: Nature has no built-in bias in favor of functionality. “Biochemical predestination” is out.

    An unexpressed segment of DNA has no way of knowing in advance: (a) whether the sequence of 100 amino acids that it codes for represents a biologically useful molecule (yes or no); or (b) how far “off base” it is, in terms of being able to code for a biologically useful protein (e.g. “just fix amino acids 17, 43, 51 and 94, and you’re done!”).

    Even if we suppose that it could eventually hit on a solution by trial and error, the problem is that there aren’t anywhere near 10^77 trials, in the history of life on Earth. Hence it seems that hitting on a DNA that could code for a viable sequence of amino acids would be tantamount to a miracle.

    Or as Francois Jacob famously put it, “the probability that a functional protein would appear de novo by random association of amino acids is practically zero.”

    Now let’s look at Helen Pilcher’s specific suggestions in the article she wrote for New Scientist (see http://evolutionarygenomics.im.....an2013.pdf ), which I cited in my post:

    (a) orphan genes arise by a process of gene duplication. Except that in the vast majority of cases they don’t, as Pilcher herself admits;

    (b) the orphan genes sit next to and slightly overlap existing, older genes, so the orphans might be able to “borrow” their switches. That doesn’t sound promising, as these are genes that code for chemically unrelated proteins – singleton, as Kozulic calls them in his 2011 Vixra article;

    (c) the protein-making factories in complex organisms are constantly churning out new proteins, allowing them to be “tested” all the time. Even if the non-coding sections of DNA are doing this, the number of trials is still way below the requisite number (10^77) for success to become likely;

    (d) there is a whole continuum of “proto-genes” which gradually gather useful mutations over time. As I understand it, there’s a certain threshold number n of amino acids, below which none of the combinations is capable of performing a useful biological function, and what’s more, n is fairly high (around 100), so the possibility of building up step by step is ruled out. Moreover, the “Methinks it is like a weasel” argument doesn’t apply here; nothing would inform the proto-gene which parts of its structure need fixing.

    Now I know you will say that a chain of argumentation is only as strong as its weakest link, but do you see what I’m getting at here? There’s a real problem, and it’s not going to go away by saying that we already know that new functional genes arise. Sure they do. But the question is: do we know that they arise by a viable natural mechanism? And that’s precisely what we don’t know. Cheers.

  79. 79
    gpuccio says:

    Evolve:

    My compliments! You understand nothing of ID and its arguments, and yet you boldly come here to give us poor fools your supreme knowledge.

    Unfortunately, I have some bad news for you.

    a) ID is about the informational problem: how does functional information in biological beings arise? You seem to believe that it arises by RV alone. That is a strange position, that even the most die hard neo darwinists usually try to avoid. Well, as VJT has already mentioned in his last answer to you, the simple problem is that there are practically zero probabilities to get the functional sequences that we observe only by RV. Try to read something about ID, and you will understand why.

    b) It’s not ID that invokes magic. It’s you that are invoking magic. How else could random variation events generate all the functional sequences of proteins (and much more)?

    c) Random genetic drift is just part of random variation. It adds nothing. Any sequence can be fixed by drift, so the probabilities of any particular sequence to be found in a random walk do not change at all because of the existence of drift. What counts is only the ratio between the target space (the functional sequences) and the search spaces (all possible sequences), IOWs, the number of states that should be tested versus the probabilistic resources of the system. And believe me, there is no game for neo darwinism without NS (well, indeed there is no game even with NS, but without it, you cannot even start to discuss!). So, take the time to read and understand what ID says, before coming here with your statements.

    So, it is true that many new genes derive from non coding sequences, as I have argued here myself, but they cannot do that by RV alone (including drift), and NS cannot act in that scenario. Therefore, only Intelligent Design can explain that kind of result.

  80. 80
    gpuccio says:

    VJ:

    About Helen Pilcher’s “suggestions”, a few brief comments:

    a) Gene duplication is only a way to transform a functional gene into non coding DNA. Functional genes cannot traverse the search space because negative NS prevents them from doing that. Non functional genes (be them non coding intergenic sequences or duplicated inactivated genes) can traverse the search space as they like, but get no help from NS, therefore they can arrive nowhere useful.

    b) I can’t see how a new protein with a new function could benefit from the “switches” of a different protein. When that happens by chance, in somatic cells, what we get is sometimes a tumor. Or just a non functional cell. And anyway, we have to have a new functional protein to use a switch. What is the use of a switch associated to a non functional sequence?

    c) I am not aware that non coding DNA is being constantly translated in cells, in the hope to get something functional from it. I suppose we should have noted that, because the proteome can be explored much more easily than the transcriptome. ENCODE has taught us that the majority of the genome is transcribed, not that it is translated. And the transcription of non coding DNA has specific functional purposes, which are mostly related to transcription regulation, and take place in the nucleus.

    d) There is no continuum of “proto genes”. We know very well that the 2000 superfamilies listed in SCOP are completely unrelated at the sequence level. What else do we need to understand that they are isolated functional islands? Small peptides are important, but they have mainly regulatory roles. The true effectors (enzymes and similar) are big molecules. Just look at the 20 aminoacyl tRNA transerases, which are extremely old and are the true effectors of transcription, IOWs the repository of the key to translate the genetic code: they are huge proteins, some of them of more than 1000 AAs, and all of them, if I remember well, of more than 500 AAs.

    That’s what neo darwinists have to explain by random variation, or by some mysterious natural selection which should have taken place before the genetic code even existed. And they accuse us of invoking magic!

  81. 81
    Timmy says:

    gpuccio #69:

    I’m not necessarily advocating or rejecting a particular copying mechanism–although admittedly it would be more convenient (from a religious perspective) if there wasn’t any common descent. What I’m mainly interested in is a method for determining whether some arbitrary similarity 1) can or 2) should be attributed to common descent, like the design inference chart that’s been promoted in other posts. So in no way am I disputing that common descent is a reasonable (let alone possible) explanation for some evidence. But before it becomes the “best possible explanation” (or best current explanation), it’s necessary to address and exclude other explanations.

    So back to what you wrote. I agree, it’s fair to say that the designer would need some kind of software repository if common descent is not involved. Although perhaps he just has an expansive memory. Who knows.

    a) No reason, necessarily. However…what you do mean by “reasonable access” to the existing copies? If you or I were going to update or modify some DNA, that would require a laboratory with a lot of specialized equipment. Which of course you would have needed in the first place, to synthesize life. In the scheme of things, throwing in some kind of data storage unit seems like a minor detail. I would sure want one, to keep track of all my original work. But who knows.

    Either way it does lead to some interesting questions about what resources the designer has at his disposal. “Why did God do it that way?” is an important question, when taken seriously and not as a childish dismissal. Unless the designer doesn’t have access to the original code, it’s not immediately apparent why he would prefer to create a new organism by using an older one (that’s been living for a while) as the starting template. It’s not like the code has improved (giggle!) or anything.

    However, maybe that is just what he did. And maybe we will never know what the reason was. Shrug.

    b) That’s fair. And if those particular modifications are truly random (and presumably within the limits of evolution) and there truly is no functional difference, then I agree it would be a strong case in favor of common descent. I don’t mean “truly” in a cheeky way, I’m just leaving the door open (as you mentioned at the end of your first response) for future discover and analysis, since it seems like we still have a long way to go. In contrast, I was impressed by the endogenous retrovirus argument for a long time–until I read (here, of course) how the choice of integration sites isn’t plainly random.

    Honestly I’m not sure what to make of varying levels in sequence homology, since I don’t know what exactly is being compared. For example I find it surprising that you could have such high levels of code variation without any difference in function. I don’t doubt the devil is in the details. As I said, I am a layman as far as genetics (and biology) goes; my degree is in ME and I have some familiarity with programming. I also have to confess I have never investigated an ID perspective on common descent (that’s what I’m doing now!), and up until now I’ve viewed it with great skepticism because the people usually promoting it are Darwinists.

  82. 82
    vjtorley says:

    Update on the possibility of chromosome 2 fusion in the human line:

    I’ve gotten some more feedback from relevantly qualified academics who were willing to “weigh in” on the case, and here’s a short summary of their findings:

    (1) Not all of them agree with Tomkins. Some do, some don’t. Of those who disagree with him, nobody is saying that chromosome 2 fusion would have been a routine affair; on the contrary, it might have been quite difficult. But some of them say we shouldn’t rule it out.

    (2) Tomkins obtained his data from ENCODE, and he claims there is clearly a functional gene transcribed across the site of the alleged fusion event. But some of the experts disputed this. One wrote: “I looked into Tomkins’ story of a gene straddling the chromosome 2 fusion site. There is indeed a transcript that straddles the site. However, it is a pseudogene, DDX11L2, which is one of a large family of 17 DDX11 pseudogenes. In this case, the first exon is distal to the fusion site.” Since DDX11L2 is one of a large family of pseudogenes, it could be argued that one more or less is not going to make a difference. Moreover, the proportion of pseudogenes that have been shown to be functional is miniscule, and the chances that all 17 pseudogenes were functional appears very remote. In short: a new transcript seems to have formed by the fusion event, but we already know that transcription occurs across the genome, and in any case, this would have been a non-functional transcript.

    (3) Some experts had claimed that there were no clear-cut cases of telomere to telomere fusion. However, there seems to be one: Ventura, M.. (2012). The evolution of African great ape subtelomeric heterochromatin and the fusion of human chromosome . Genome Research, 22(6). See also this paper: Giannuzzi, G.. (2013). Hominoid fission of chromosome 14/15 and the role of segmental duplication. Genome Research, 23(11).

    (4) The argument that if chromosomes did fuse spontaneously, we should see it all the time, does not apply here, as this is not a simple joining of ends. The postulated event was not a real case of telomere-to-telomere fusion. Instead, it was more of a recombination event that lopped off most telomeric sequences, rather than a fusion event. See http://genome.cshlp.org/content/22/6/1036.long .

    (5) What’s more, there’s evidence of a degenerate centromere in humans at the location where the other chimp chromosome 2 has a centromere.

    (6) However, the fusion of the 2 chromosomes would have had to have been accompanied by the simultaneous loss of the other centromere, which is unlikely, but by no means impossible.

    (7) The argument that this can’t be a fusion event because it’s degenerate, is a circular one.

    On the other hand:

    (1) Perhaps the real reason that only a miniscule proportion of pseudogenes have been identified as functional is that no-one even bothers to look for a function, because they are already convinced by evolutionary dogma that there won’t be any function.

    (2) Non-essential doesn’t mean non-functional.

    (3) A problem with degeneracy still remains: when are these alleged alterations from the normal telomere (i.e. mutations) occurring, and why do they occur at a high frequency only before they get propagated to the entire human population?

    (4) Why isn’t the occurrece of fusion hypervariable, across the human population? The fact that it isn’t, argues against fusion.

    They’re the key points. Please bear in mind that I’m not a geneticist, so I can’t offer any opinions of my own here. However, it seems to me that Tomkins has not yet made a knock-down case for the impossibility of the alleged fusion event leading to chromosome 2 in the human line. So far, it’s a verdict of “Case not proven,” as the Scots say. Cheers.

  83. 83
    Evolve says:

    VJTorley @58

    ///ENCODE is right.
    Tomkins pulls the data from ENCODE and there is clearly a gene transcribed across the fusion event. The gene is rather larger than the 1500 bp that Miller quotes. The gene is a helicase (if I remember correctly) expressed in various tissues throughout development. If you read Tomkins’ paper, he demonstrates where the supposed telomere ends are located, where additional centromeres are supposedly located, and how the region is transcriptionally active (a hallmark associated with non-telomeric DNA).///

    I’ll reserve judgement on the exact location of the DDX11L2 gene in relation to the fusion site, since that needs to be cross-checked in detail. But there are other points Tomkins ignores and misrepresents:

    The DDX11L2 gene present on human chromosome 2 is part of the DDX11L gene family, members of which are present in humans as well as other apes. These are homologous genes sharing evolutionary ancestry and they arose by duplication events.

    The following paper by Costa et. al reports that the human DDX11L genes share 98% sequence homology to that of chimps and 91% to that of rhesus monkey.
    Fig. 3 in the same paper shows that the chimp and gorilla DDX11L genes are detectable using probes derived from a human version of the gene, further underlining their homology. Moreover, DDX11L genes exclusively localize to the ends of chromosomes in all the apes examined:

    http://www.biomedcentral.com/c.....10-250.pdf

    Thus, the presence of a DDX11L gene in the middle of human chromosome 2 makes perfect sense, if these genes are exclusively located at chromosome ends and human chromosome 2 was produced by the end-to-end fusion of two ancestral ape chromosomes. Tomkins ignores these observations because they directly contradict his claims, although he quotes the paper to cherry-pick what he wants!

    Tomkins tries to salvage the situation by saying chimps don’t have DDX11L2 in their corresponding chromosomal end portions. But chromosomal ends are well known to be highly unstable & dynamic areas that undergo deletions, duplications & inversions. So, chimps could have simply lost their DDX11L2 versions or these genes may have jumped on to other chromosomes.

    Tomkins further explains in length how human DDX11L2 is transcribed, has transcription factor binding sites and microRNA binding sites. But all these still do not indicate there’s a functional RNA or protein product! The transcript produced can simply be noise. Such spurious transcription is widespread as even Tomkin’s pet data, ENCODE, shows. Tomkins doesn’t attempt any experiments to identify or characterize the RNA/protein product under question at, despite repeatedly assuming & claiming that the gene is functional!

    Now, even if a functional protein product is identified for DDX11L2, it can be due to neo-functionalization of the pseudogene. Some pseudogenes may acquire novel functions as they accumulate mutations. This is hardly unknown or surprising.

    Tomkins mostly focuses on the fusion site. But he also tries to dismiss the massive similarity found along the length of human chromosome 2 and its counterparts in apes, by invoking a kind of common design argument. But, there too, he fails to account for the presence of increasing disparity in banding pattern with increasing distance between species, exactly as predicted by evolution.

    See Fig. 2 in the following paper:
    http://genome.cshlp.org/content/12/11/1651.long

    Human chromosome 2 banding pattern is most similar to that of chimps, slightly less similar to that of gorillas and still less to that of orangutans.

    There’s a reason why Tomkins published his piece in a creation journal and not in a proper science journal, where his dubious claims would have prevented it from getting past peer-review.

  84. 84
    CentralScrutinizer says:

    Evolve: I don’t get you. The well-understood mechanisms of mutation, natural selection, random genetic drift and neutral theory explain the evolution of all life that we know of, including humans.

    Care to provide a gap-free account of the emergence of any cell type, tissue type, organ or body plan using these “mechanisms of mutation, natural selection, random genetic drift and neutral theory” that isn’t actually a degradation (e.g. cancer cells) ?

    Thanks

  85. 85
    Joe says:

    Genetic similarity can be accounted for via a common design or convergence. However it still remains that the alleged fusion occurred in the human lineage and therefor had nothing to do with any alleged common ancestor with chimps.

    Human Chromosome 2 From a Design Perspective

  86. 86
    Evolve says:

    guccio @ 79

    ///So, it is true that many new genes derive from non coding sequences, as I have argued here myself, but they cannot do that by RV alone (including drift), and NS cannot act in that scenario. Therefore, only Intelligent Design can explain that kind of result.///

    I addressed this already. Your creation model utterly fails to explain why the Poldi gene (I cited above) has more functional mutations in closely-related mice species, but less functional mutations in distantly-related rats and still less functional mutations in even more distantly related humans.
    The gene is not expressed in both rats & humans, so what was the designer doing with making the rat version look more similar to mice than the human version?! He probably wanted to make it look as if evolution happened!

    I hope you realize the fallacy of your ID argument.

  87. 87
    bornagain77 says:

    Evolve, I know you think you got evolution all ‘scientifically proven’ with all your genetic similarity evidence, (all the while neglecting to mention very similar sequences in highly divergent species, Bats and Whales for instance), but, call me a skeptic if you will, but could you be so kind as to actually show us a demonstration of this awesome Darwinian mechanism in action? It would go a long way towards helping you make your case that what you believe to be true, that material processes can generate highly integrated information in genomes, actually is true!

    The Law of Physicodynamic Insufficiency – Dr David L. Abel – November 2010
    Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.”
    http://www-qa.scitopics.com/Th.....iency.html

  88. 88
    CentralScrutinizer says:

    The gene is not expressed in both rats & humans, so what was the designer doing with making the rat version look more similar to mice than the human version?! He probably wanted to make it look as if evolution happened!

    You seem to be operating under the assumption that ID means “no evolution.” It doesn’t. Most ID proponents are not young earth creationists. Many of the leading lights of ID accept common descent. The issue is the source of information for certain biological features which the modern evolutionary synthesis is utterly deficient to explain.

    You could start by reading this:

    http://www.uncommondescent.com/id-defined/

  89. 89
    Joe says:

    Evolve:

    Your creation model utterly fails to explain why the Poldi gene (I cited above) has more functional mutations in closely-related mice species, but less functional mutations in distantly-related rats and still less functional mutations in even more distantly related humans.

    You don’t even understand the creation model. And unguided evolution doesn’t even have a model.

    Evolve doesn’t realize that his position doesn’t even have an argument.

  90. 90
    Evolve says:

    VJ Torley @ 78

    ///An unexpressed segment of DNA has no way of knowing in advance: (a) whether the sequence of 100 amino acids that it codes for represents a biologically useful molecule (yes or no); or (b) how far “off base” it is, in terms of being able to code for a biologically useful protein (e.g. “just fix amino acids 17, 43, 51 and 94, and you’re done!”).
    Hence it seems that hitting on a DNA that could code for a viable sequence of amino acids would be tantamount to a miracle.
    there is a whole continuum of “proto-genes” which gradually gather useful mutations over time. As I understand it, there’s a certain threshold number n of amino acids, below which none of the combinations is capable of performing a useful biological function, and what’s more, n is fairly high (around 100), so the possibility of building up step by step is ruled out. Moreover, the “Methinks it is like a weasel” argument doesn’t apply here; nothing would inform the proto-gene which parts of its structure need fixing. ///

    First of all, generation of novel information does not require tons of new genes. New information can readily emerge by the rewiring & re-purposing of existing genes & gene regulatory networks. This is why the number of genes across species are not THAT different.

    Why do you guys insist that DNA should always code for a viable, functional sequence that too with all the mutations required for it happening in one lockstep? This is where you’re horribly going wrong. A gene need not have any function at all to linger on in our genomes. Such useless genes and DNA sequences will persist over many generations as long as they don’t have significant deleterious effects. That’s why we all carry around tons of pseudogenes, transposons and other junk DNA.
    Without such a huge buffer of useless DNA, our species wouldn’t have survived for long, since mutational load on functional sequences would break our metabolism and kill us sooner than later.

    Over time these useless DNA will accumulate mutations, many of which could be neutral, meaning that the new mutations also don’t impart any particular effect. But in the backdrop of these neutral mutations, further mutations could produce a viable effect – and lo & behold now we’ve a functional gene!
    There are all kinds of other possible scenarios. For eg: existing genes can duplicate, one copy may continue to function normally while the other copy is free to pick up mutations slowly over time and finally produce something with a different function. All these occur by well-known natural processes.

  91. 91
    bornagain77 says:

    Evolve,, what no actual empirical evidence? Just a bunch of conjecture about what could have and should have happened? Certainly you got something? This is science man, show me your goods!

  92. 92
    CentralScrutinizer says:

    Evolve: There are all kinds of other possible scenarios. For eg: existing genes can duplicate, one copy may continue to function normally while the other copy is free to pick up mutations slowly over time and finally produce something with a different function. All these occur by well-known natural processes.

    Fine. Show us a gap-free account of the emergence of any cell type, tissue type, organ or body plan using these “well-known natural processes” that isn’t actually a degradation (e.g. cancer cells). And after that, we can talk about the origin of protein domains.

    Thanks

  93. 93
    CentralScrutinizer says:

    Graham2: Religion poisons everything.

    All religion?

    Do you consider deism a religion? That is, is there mere belief in a creator religious?

    If so, how does a such a belief poison anything?

  94. 94
    Joe says:

    sock puppet:

    All these occur by well-known natural processes.

    Hey our computers operate via well known natural processes. But that doesn’t mean that the blind watchmaker produced them.

  95. 95
    Evolve says:

    VJTorley @ 82,

    ///A problem with degeneracy still remains: when are these alleged alterations from the normal telomere (i.e. mutations) occurring, and why do they occur at a high frequency only before they get propagated to the entire human population?///

    This is yet another non-issue.
    Telomeres normally occur at the ends of chromosomes where enzymes called telomerases constantly renew the telomeres. This is important because telomeres tend to mutate and get lost quite easily.
    Shortened telomeres are vulnerable to fusion as shown by the following study:

    http://www.cell.com/retrieve/pii/S0092867401800064

    Therefore, it’s hardly surprising that the telomeres present in the middle of human chromosome 2 (as a result of the fusion event) are quite short. And since they’re now in the middle of the chromosome, telomerases are unable to renew the telomeres anymore. So they start accumulating mutations at a rapid pace and become degenerate. It is known that telomere sequences are hotspots for mutation.
    See: http://www.nature.com/nature/j.....04029.html

  96. 96
    gpuccio says:

    Timmy:

    Thank you again for your very honest comments. It’s really a pleasure to discuss with you.

    I am perfectly comfortable with your position, both in point a) and in point b). I would only add that maybe acting on existing beings is the natural way for the designer, even if he has a repository of software, or simply a good memory. I am confident that facts will gradually help us decide, maybe never a final decision (science is not the place of absolute truth), but a reasonable evaluation.

    I must confess that I have no detailed opinion about endogenous retroviruses, because there are many variables involved, and I don’t know the topic well. Instead, I am very impressed by the homologies and differences in protein sequences, also because I have checked many of them personally, through the Blastp tool.

    I can maybe give you some further details about the problem of sequence/structure/function relationship in proteins.

    Let’s take as an example myoglobin, which is one of the most studied globular proteins. In humans, it is a protein rather simple, of 154 AAs, with a definite structure and function. In UNIPROT, its ID is P02144, and its function is described as follows:

    “Serves as a reserve supply of oxygen and facilitates the movement of oxygen within muscles”

    Here is the blast alignment between human myoglobin and the myoglobin in Tunnus Atlanticus (tuna fish):

    Score 123 bits(308)
    Expect 2e-40
    Identities 68/148(46%)
    Positives 88/148(59%)
    Gaps 3/148(2%)

    and here is the blast alignment between human myoglobin and the myoglobin in the mouse:

    Score 264 bits(674)
    Expect 2e-95
    Identities 129/154(84%)
    Positives 141/154(91%)
    Gaps 0/154(0%)

    As you can see, we have 84% identities in the mouse, and only 46% in the tuna fish. And yet, the protein length is almost the same, and the protein function is the same. The fact is, even the protein structure is more or less the same (with possible minor functional differences).

    IOWs, sequence can change, while still showing impressive homology (the 46% identities in tuna still correspond to an expect value of 2e-40, which means that we can safely exclude that the similarities are random), and still the homologue proteins can retain their structure and function even with great differences in sequence.

    There are many reasonable explanations for that. The main are:

    a) Many substitutions are almost neutral to the protein structure and function. That’s why the “Positives” percent if higher than the “Identities” percent.

    b) Substitutions which would change the protein structure can be “compensated” by other substitutions, so that the general structure remains similar.

    These are very general concepts. That’s why the study of protein functional space is so difficult. We must be grateful to those good biologists and scientists, including “our” scientists like Axe and Durston and others, who are working at that.

  97. 97
    bornagain77 says:

    Evolve, we know that Darwinian processes are excellent at breaking things.

    Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 – May 2013
    Excerpt: It is almost universally acknowledged that beneficial mutations are rare compared to deleterious mutations [1–10].,, It appears that beneficial mutations may be too rare to actually allow the accurate measurement of how rare they are [11].
    1. Kibota T, Lynch M (1996) Estimate of the genomic mutation rate deleterious to overall fitness in E. coli . Nature 381:694–696.
    2. Charlesworth B, Charlesworth D (1998) Some evolutionary consequences of deleterious mutations. Genetica 103: 3–19.
    3. Elena S, et al (1998) Distribution of fitness effects caused by random insertion mutations in Escherichia coli. Genetica 102/103: 349–358.
    4. Gerrish P, Lenski R N (1998) The fate of competing beneficial mutations in an asexual population. Genetica 102/103:127–144.
    5. Crow J (2000) The origins, patterns, and implications of human spontaneous mutation. Nature Reviews 1:40–47.
    6. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501.
    7. Imhof M, Schlotterer C (2001) Fitness effects of advantageous mutations in evolving Escherichia coli populations. Proc Natl Acad Sci USA 98:1113–1117.
    8. Orr H (2003) The distribution of fitness effects among beneficial mutations. Genetics 163: 1519–1526.
    9. Keightley P, Lynch M (2003) Toward a realistic model of mutations affecting fitness. Evolution 57:683–685.
    10. Barrett R, et al (2006) The distribution of beneficial mutation effects under strong selection. Genetics 174:2071–2079.
    11. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501.
    http://www.worldscientific.com.....08728_0006

    Mutations and Darwinism – Dr Jerry Bergman – June 2013 – video
    http://www.youtube.com/watch?v=pfgiAWBluxE

    What we want to know is if Darwinian processes can create anything!

    Macroevolution, Good Science, and Redeeming Mathematics – Kate Deddens – February 2012
    Excerpted quote: As obviously designed as a spaceship or a computer…Evolutionary biologists have been able to pretend to know how complex biological systems originated only because they treated them as black boxes. Now that biochemists have opened the black boxes and see what is inside, they know the Darwinian theory is just a story, not a scientific explanation…
    (Phillip E. Johnson, Defeating Darwinism, Downers Grove, IL: InterVarsity Press, 1997, 77-78.)
    http://www.classicalconversati.....atics.html

    “There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system only a variety of wishful speculations. It is remarkable that Darwinism is accepted as a satisfactory explanation of such a vast subject.”
    James Shapiro, molecular biologist, National Review, Sept. 16, 1996

    EVOLUTIONARY JUST-SO STORIES
    Excerpt: ,,,The term “just-so story” was popularized by Rudyard Kipling’s 1902 book by that title which contained fictional stories for children. Kipling says the camel got his hump as a punishment for refusing to work, the leopard’s spots were painted on him by an Ethiopian, and the kangaroo got its powerful hind legs after being chased all day by a dingo.
    Kipling’s just-so stories are as scientific as the Darwinian accounts of how the amoeba became a man.
    Lacking real scientific evidence for their theory, evolutionists have used the just-so story to great effect. Backed by impressive scientific credentials, the Darwinian just-so story has the aura of respectability.
    Biologist Michael Behe observes:
    “Some evolutionary biologists–like Richard Dawkins–have fertile imaginations. Given a starting point, they almost always can spin a story to get to any biological structure you wish” (Darwin’s Black Box).,,,
    http://www.wayoflife.org/datab.....ories.html

    “Grand Darwinian claims rest on undisciplined imagination”
    Dr. Michael Behe – 29:24 mark of following video
    http://www.youtube.com/watch?f.....fM#t=1762s

  98. 98
    gpuccio says:

    Evolve says:

    Over time these useless DNA will accumulate mutations, many of which could be neutral, meaning that the new mutations also don’t impart any particular effect. But in the backdrop of these neutral mutations, further mutations could produce a viable effect – and lo & behold now we’ve a functional gene!

    That is exactly a good example of the non scientific reasoning I outlined in my post #79. I don’t see where you are addressing the informational and probabilistic problem.

    I addressed this already. Your creation model utterly fails to explain why the Poldi gene (I cited above) has more functional mutations in closely-related mice species, but less functional mutations in distantly-related rats and still less functional mutations in even more distantly related humans.
    The gene is not expressed in both rats & humans, so what was the designer doing with making the rat version look more similar to mice than the human version?! He probably wanted to make it look as if evolution happened!

    I don’t understand your point. The gene is functional only in mice, the variations in rats and humans are almost surely the result of RV. Instead, the function in mice, if properly studied, will probably warrant a design inference.

    Just to clarify your ideas, please remember the following important points:

    a) The designer does not control everything. RV exists, and is not designed. However, it cannot generate new complex functional information. Complex functional information is designed.

    b) If with “evolution” you mean the (non functional) results of RV, that kind of “evolution” certainly happens. It’s not that the designer wants to “make it look as if evolution happened”. Non functional change happens all the time. It’s not the result of design.

  99. 99
    gpuccio says:

    BA:

    I see that you had already made my point. Well, twice is better than once.

  100. 100
    Upright BiPed says:

    Hi GP,

    …it cannot generate new complex functional information…

    “It” (neither RV nor NS) doesn’t have what it takes to establish the onset of any information at all.

    I (of course) recognize that (at the pleasure of our materialist adversaries) these dialogues simply assume the translation system (because they have absolutely zero explaination for it) but it doesn’t hurt to occasionally circle back to the facts on the ground.

    Darwinian evolution simply assumes the very organization it requires to exist.

    (I’ll go back to lurking now:) )

  101. 101
    junkdnathewhite says:

    ‘Without such a huge buffer of useless DNA, our species wouldn’t have survived for long, … ‘

    This statement seems to be self-refuting.

  102. 102
    Joe says:

    This statement seems to be self-refuting.

    You just don’t understand evolutionism. 😎

  103. 103
    JGuy says:

    Roy @ ^^^-somewhere up there-^^^

    Now this is a particularly interesting accusation for you, a Darwinist, to make, since Darwinists are notorious for smuggling in information into their evolutionary algorithms (i.e. Dawkins’ targeted Weasel phrase).

    “Smuggling”?

    Dawkins stated up-front exactly how the program worked and where the target string came from. If you think that’s smuggling, you’re deluded.

    Roy

    Just because a person implicitly & unwittingly confesses to his contraband cargo doesn’t mean he’s not smuggling that something.

  104. 104
    JGuy says:

    Evolve.

    Would appreciate your help. Can you help direct me to where I can find any chimp genome sequence online? Let me qualify that… not the one that has been constructed using the human genome as a framework to fit/hang sequence segments… But what I’m looking for is a fully untainted chimp genome sequence done without reference for sequence alignment based on any other genome like the human genome.

    Since the billion(s?) dollar human genome project, costs have dropped radically into the hundreds (cool!), and a pure/fresh/from scratch/ chimp genome should be available online.

    I’d like to compare it to the human genome which actually has been sequenced in that way.

    Thanks for any help. I’m sure a lot of folks here would appreciate that help too.

  105. 105
    JGuy says:

    Why would it matter if humans had a fused chromosome anyway?

    First of all, that would mean there was a fixation at a bottle neck. Either that, or it has no clear advantage and if it has no bearing on mating compatibility, we should see a mix of fused and unfused chromosomes in the human population.

    Anyway.

    Would it be more consistent with common ancestry if humans and chimps had the exact same number of chromosomes? I think it would be better, and perhaps this is actually a fight from evolutionists because they need it to be fused.

    Meanwhile, fused or unfused has no other significance in the debate that I see.

  106. 106
    Evolve says:

    I forgot to say something in my post # 83 regarding Tomkins’ take on chromosome 2 fusion. The Costa et. al paper I mentioned analyzed chromosomes from 3 human individuals. In one case the DDX11L2 gene was located at the end of chromosome 2, far away from the fusion site in the centre! Such variation in localization was also detected for DDX11L genes on chromosomes 9 and X. Their Fig. 3 shows this. It highlights the widespread rearrangements occuring in the subtelomeric regions, which Tomkins has conveniently ignored.

  107. 107
    Evolve says:

    ///Why would it matter if humans had a fused chromosome anyway?///

    It doesn’t matter if humans have fused or unfused chromosomes. And no evolutionary biologist has a pressing need for a fused chromosome.

    After all, all human unfused chromosomes can still be aligned with the corresponding ape chromosomes showing their similarities.

    What matters is that we see one pair less chromosomes in humans compared to the other great apes. This is an observation and this observation could challenge the theory that they all are related.

    It is under this context that the fused chromosome assumes relevance. Fusion accounts for the missing pair of chromosomes and evolutionary theory still stands.

  108. 108
    Evolve says:

    gpuccio @ 98,

    ///Complex functional information is designed.///

    This is a baseless argument with no supporting evidence.

    The random variation we observe is not just a garbled mess, there’s a pattern to it. Your model must be able to explain that pattern. Ignoring the data and simply stating that something appears complex & improbable, and therefore designed, won’t work.

    Here’s the figure from the Poldi gene paper I was talking about:

    [url=http://postimage.org/][img]http://s17.postimg.org/8qodvzs9b/image.jpg[/img][/url]
    [url=http://postimage.org/]jpg images[/url]

    http://postimg.org/image/aihcqwbm3/

    The functional Poldi gene is only present in some species of mice. However, the framework for this gene is also present in other mice as wells as in rats & humans, where of course it is not functional.
    If God’s intention was to create a new gene in some mice, then why is the framework present in rats & humans at all? Your creation model spectacularly fails there itself. It’s clear that all these species evolved from a common ancestor which explains why all of them have the framework.

    Starting with humans we can see that they vary the most in relation to the mice carrying the gene. Humans have the least number of functional regions in the framework (4 red crosses). Thus humans must be the most distantly related species to those mice.

    Next up, rats show less variation than humans. They have a few more functional regions in their framework, but still not all that’s required to produce the new gene (2 red crosses). Therefore rats must be closer to mice than humans.

    Coming to the various mouse species, basal (more ancient) mice lack one functional region to produce the gene (1 red cross). Thus they are closer than rats to the mice carrying the gene.
    Finally, in more recent mouse species, the gene has emerged with all functional regions (no red crosses, all green ticks). These species are the closest relatives of the lot.

    This family tree has already been established by other studies. Now the emergence of this gene agrees with it and exhibits the same pattern. We can trace how this new gene emerged through related lineages and through what steps.
    This is just one among innumerable examples we have in biology showing the explanatory power of evolutionary theory. A creation model miserably fails to account for this pattern of variation. As I said, if God wanted to create a new gene in some mice, then why does this DNA exist at all in other species and why do they show this pattern?

  109. 109
    Upright BiPed says:

    This is a baseless argument with no supporting evidence.

    Do you not, against universal evidence to the contrary, simply assume that material processes can establish the semiotic translation system that your analysis depends upon?

  110. 110
    Joe says:

    Evolve- your position cannot explain mice. So tat would be a problem for your “model”. Well blind watchmaker evolution doesn’t even have a model.

  111. 111
    Joe says:

    Evolve has serious problems to deal with, namely:

    Blind watchmaker evolution cannot account for telomeres and it cannot account for chromosomes, eukaryotes and meiosis.

  112. 112
    Roy says:

    Just because a person implicitly & unwittingly confesses to his contraband cargo doesn’t mean he’s not smuggling that something.

    Sheesh. Since when was Dawkins’ description of his algorithm implicit, unwitting or confessional?

    If Dawkins had tattooed his code on your forehead you’d be complaining that Dawkins hadn’t stood you in front of a mirror.

    Roy

  113. 113
    Upright BiPed says:

    Roy,

    The idea that mankind needed a toy to demonstrate that cumulative seletion can reach a target in a reasonable timeframe is an insult to intelligence and an embarrassment to science. The toy was presented for the purpose of bullshitting the public. End of story.

  114. 114
    JGuy says:

    Evolve @ 107

    It doesn’t matter if humans have fused or unfused chromosomes. And no evolutionary biologist has a pressing need for a fused chromosome.

    In the context of the ID evolution debate is my question. And it is often presented, it seems, as a powerful argument for evolution – but that isn’t really the case. No better than if humans and chimps had the exact same number of chromosomes. After all, one could reason from merely using comparative anatomy, which predates Darwin even, to surmise the chromosomes are fused. I’m not saying that it is, I’m just saying the notion has no need of common descent intrinsically.

    After all, all human unfused chromosomes can still be aligned with the corresponding ape chromosomes showing their similarities.

    Does this mean you could help me out with finding a pure sequence per my request of you in comment #104?

    What matters is that we see one pair less chromosomes in humans compared to the other great apes. This is an observation and this observation could challenge the theory that they all are related.

    It is under this context that the fused chromosome assumes relevance. Fusion accounts for the missing pair of chromosomes and evolutionary theory still stands.

    That’s what I was thinking. It’s not so much an observation that should be used against those that might evolution, it’s more of a necessary interpretation of the data to try to save evolution from the consequence – specifically Darwin’s description of common descent.

  115. 115
    wd400 says:

    JGuy,

    There is tonnes of raw sequencign data from chimps – but you aren’t going to like it.

    Junkdnathewhite

    Without such a huge buffer of useless DNA, our species wouldn’t have survived for long, … ‘

    This statement seems to be self-refuting.

    How so? The wording is a little off perhaps, but I dont’ see how the statement refutes itself.

  116. 116
    JGuy says:

    wd400,
    Thanks. Lot’s of segments can be found there it seem, but for whole genome comparison of chimps (other than pygmy chimps to animals other than human). I’d probably not enjoy playing with that many puzzle pieces. 😛

    From that list, there was one result (in 21 pages) that I found pertaining to a whole genome comparison of genetic differences between humans and chimps.

    Submitted 25 October 2013:
    http://www.ncbi.nlm.nih.gov/sra/ERX027262

    I’m not familiar with how to look into this, so I can’t see the experiment to see any summary of results. Perhaps, they are not public.

    Something yet to be released (not sure how related it is, but it came up in the results for whole genome comparisons):
    http://www.ncbi.nlm.nih.gov/sra/ERX027263

  117. 117
    tjguy says:

    Just read that ICR is in the process of doing a new study comparing the genomes of apes and humans.

    Of the genes that are found in both species, evolutionists have only reported on the sub-segments of the genes that are similar. Because of these highly selective studies, we really don’t know how similar human genes are to ape genes because non-similar data were discarded. Therefore, an extensive study is in progress at the Institute for Creation Research to compare a wide variety of primate gene data sets against a comprehensive database of known human gene variants.

    [I’m excited about this study as I fully expect it to challenge the idea of common descent and validate Tompkins research.]

    So how does a scientist extract only the gene-based information from a genome? When protein-coding genes are active, they produce RNA copies of genes called transcripts or messenger RNAs (mRNA) that are used by the cell to make proteins. Using specialized techniques, these mRNAs can be captured and then sequenced. The mRNA sequences from one organism can then be compared to that of another to gauge how similar the genes are.

    To create an exhaustive database of human genes, the DNA sequences of nearly nine million different human mRNA variants were downloaded from the National Center for Biotechnology Information (NCBI) public database. Even though the human genome is thought to only contain about 22,000 genes, many different gene variants can be produced through a process called alternative splicing. (4) After setting up the target human gene database, query data sets containing the gene sequences from a diversity of primates were also downloaded.

    Although the study is just beginning, interesting patterns are beginning to emerge that challenge the standard evolutionary model of human origins. First, it looks as though all apes and monkeys contain significant portions of their genes that are very similar to parts of human genes. However, the primate genes also contain significant sections that are specific to their kind (e.g., chimp, gorilla, orangutan, etc.) that are not found in human genes.

    While we are early in the research, the similarity in the statistics and patterns observed are not supportive of the standard Darwinian evolutionary dogma. Instead, the mosaic-type picture starting to emerge is that humans, along with each type of primate, were uniquely created “after their kind.”

    Because of similarities in physiology and overall general anatomical features between humans and primates, certain sections of programming code (DNA sequence) have been repeated—a logical prediction for any type of engineered system.

    http://www.youroriginsmatter.com/conversations/view/how-similar-are-humans-apes/215

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