DNA Scrambles Darwin's Tree

Evolution News & Views September 15, 2012

Darwin's tree of life might be visible in DNA, if DNA didn't conspire to scramble the signal.

Now that quite a few genomes have been published, a team from Australia and France went on a Darwin fishing trip in the gene pool. In the largest study of its kind to date, they examined microsatellite markers (tandem-repeated DNA motifs of 1-6 base pairs) that are widespread in eukaryotic genomes. If neo-Darwinism is correct, these non-coding stretches of DNA should reflect the tree of common ancestry by showing similar mutational patterns in related groups.

Well, they don't. The paper by Meglecz, Neve, Biffin and Gardner in PLoS ONE is titled, "Breakdown of Phylogenetic Signal: A Survey of Microsatellite Densities in 454 Shotgun Sequences from 154 Non Model Eukaryote Species." What went wrong?

As the title implies, the team checked 154 "non-model" species. Darwinian evolutionists tend to focus on the model species, like a particular roundworm, the fruit fly Drosophila melanogaster, and a species of watercress, because their genomes are complete and most researchers use them in experiments. Problem: they may or may not be representative:

Although information for model species is accumulating rapidly, it is insufficient due to a lack of species depth, thus intragroup variation is necessarily ignored. As such, apparent differences between groups may be overinflated and generalizations cannot be inferred until an analysis of the variation that exists within groups has been conducted. In this study, we examined microsatellite coverage and motif patterns from 454 shotgun sequences of 154 Eukaryote species from eight distantly related phyla (Cnidaria, Arthropoda, Onychophora, Bryozoa, Mollusca, Echinodermata, Chordata and Streptophyta) to test if a consistent phylogenetic pattern emerges from the microsatellite composition of these species.

Sounds like a good test. After all, scientists shouldn't generalize on overinflated signals, right? The team expected to find nicely behaved data interpolated between the model species. It wasn't to be:

It is clear from our results that data from model species provide incomplete information regarding the existing microsatellite variability within the Eukaryotes. A very strong heterogeneity of microsatellite composition was found within most phyla, classes and even orders. Autocorrelation analyses indicated that while microsatellite contents of species within clades more recent than 200 Mya tend to be similar, the autocorrelation breaks down and becomes negative or non-significant with increasing divergence time. Therefore, the age of the taxon seems to be a primary factor in degrading the phylogenetic pattern present among related groups. The most recent classes or orders of Chordates still retain the pattern of their common ancestor. However, within older groups, such as classes of Arthropods, the phylogenetic pattern has been scrambled by the long independent evolution of the lineages.

There are two ways to interpret this anomaly. One is that microsatellites mutate too fast to maintain the phylogenetic signal. (This is known as a "post hoc rationalization.")

The other is that Darwin was wrong. Data do not show a phylogenetic pattern; they show common design with some variation.

Well, Darwinists are not ones to allow a little data to get in the way of their grand scenario. "The origin and spread of microsatellites within a genome is a puzzling question," the researchers say, couching solutions in a nebulous future: someday, someone may figure out how they evolve. "A more thorough understanding of factors influencing the genomic distribution of microsatellites would facilitate their continued use as a molecular marker and contribute to a general understanding of microsatellite evolution in genomes," they rationalize. Maybe they arise de novo by point mutations then elongate. Maybe they spread by transposable elements.

For one thing, chance is out: "Microsatellite formation cannot be explained by chance alone, since the expected density of microsatellites, assuming random association of DNA bases, is far lower than their observed genome wide density," they confess. Does this suggest some functional principle in microsatellites? (Remember, this paper preceded the publication of the ENCODE project.)

They do claim partial success. Most of the vertebrate class data was not as "heterogeneous" (scrambled) as in other taxa. They claim that this shows scrambling increases with time; the data were less scrambled for species evolving within the last 200 million years, they say. However, it was very scrambled for arthropods over the same time frame. And even the "conserved phylogenetic pattern" for vertebrates could be a false positive. Why? Because earlier surveys using fewer species produced patterns that evaporated in their survey with more species:

Thus, by increasing the number of species studied for each phylogenetic group, considerable heterogeneity is observed in microsatellite composition and coverage. This is a very important take home message from this study.

So no clear pattern can be claimed in their study either. Even within certain vertebrate classes (e.g., birds), some outlier species had very different microsatellite compositions. Overall, "no general pattern emerged," they say. "Just as total microsatellite coverage varied within classes and orders, motif length proportions can be markedly different between even closely related species."

This is hard to explain in either a design paradigm or a Darwinian one. Why would a designer make closely related species so completely different in their microsatellite composition? More on that in a minute.

How's this for covering your bases:

Both the presence and absence of such a phylogenetic signal are likely to throw light on the evolution of microsatellites. For example, evidence for the maintenance of inherent differences between major evolutionary groups invokes a varied yet functional contribution of these repetitive elements within disparate genomes. Alternatively, inconsistencies within lineages call for a greater role of random processes for explaining microsatellite distributions.

Darwinian evolution can't lose. If the signal is there, it evolved! If it's not there, it evolved!

Aren't Darwin skeptics permitted to call foul here? Darwinian theory predicts phylogenetic patterns. What better place to look than in DNA? If mutations spread in the gene pool over time, and nature selects any beneficial mutations, or doesn't eliminate neutral genetic drift, why wouldn't there be a phylogenetic signal in both genes and non-coding regions? It's a little late to make excuses after the data are in.

Design researchers, by contrast, might be surprised at the variations, but not worried. They had no need to predict a phylogenetic pattern. ID advocates could accept quite a bit of variation by epigenetic coding algorithms that respond to environmental cues. It's not a showstopper, as it should be for neo-Darwinism. In fact, it might be a motivator instead: let's explore the functional significance of the variations.

In their conclusion, the authors warn fellow Darwinists about sample bias: "Sampling of the rest of the Eukaryotes was insufficient to reveal a phylogenetic pattern, but even with limited information, we could clearly point out that generalizing information of microsatellite content from few species to a whole group can only be justified if they are from a very recent clade."

The authors are very adept at listing all the possible reasons (excuses) for their failed prediction. Readers can explore these at their leisure in the Discussion section of this open-access paper. What's clear, though, is that the Darwin fishing expedition came back empty, with a lot of fish stories about the one that got away.

- See more at: http://www.evolutionnews.org/2012/09/dna_scrambles_d064341.html#sthash.UuzMxhS5.dpuf

At Why Evolution Is True, Jerry Coyne Is Strangely Silent on the ENCODE Results

David Klinghoffer September 20, 2012 

I noted earlier, referring to Richard Dawkins, the general rule that being a Darwinist means never having to say "I was wrong." Here's another case in point.

On the topic of ENCODE's evisceration of the idea of pervasive junk DNA, the normally boisterous Jerry Coyne at Why Evolution Is True has been strangely quiet. In fact Coyne hasn't mentioned the news at all -- by far the biggest news (of any relevance to evolution) out of the world of science in years. He has instead followed the solid principle that when you feel the need to fill an awkward silence on your Darwinian-atheist blog, rather than addressing a ticklish scientific challenge to your views, just go ahead and make fun of Islam.

There's an easy target. What would we do without it?

Perhaps I missed something at WEIT, but there seems to be not a single mention of ENCODE since the story hit; see here for the search results.

Maybe this is because in his 2009 book Why Evolution Is True, Dr. Coyne gives it as a prediction of neo-Darwinism that the genome should be replete with inactive, functionless "dead genes." This is Coyne's approximate equivalent of what's called elsewhere "junk DNA." He's got a whole section on it, starting at page 71.

Our genome -- and that of other species -- are truly well-populated graveyards of dead genes.

He triumphs about how only evolution can explain this state of affairs, whereas appeals to design are stymied by it. Surely this calls for a clarification from Professor Coyne, in light of the news about ENCODE. Yet as I said, Coyne is silent as, well, a graveyard. Hm, wonder why? 

- See more at: http://www.evolutionnews.org/2012/09/at_why_evolutio064541.html#sthash.bSUKJvXO.dpuf

In Debate, Britain's Chief Rabbi Tweaks Richard Dawkins with the Myth of "Junk DNA"

David Klinghoffer September 20, 2012 

This is delightful. In a BBC-sponsored debate with Richard Dawkins, Britain's chief rabbi, Lord Jonathan Sacks, tweaked Dawkins with the ENCODE project results. He does it right out of the box, in the opening moments of the encounter, observing that whereas until recently 98 percent of the genome was "dismissed as junk DNA, " "actually that 98 percent that people thought was junk isn't junk at all. It's absolutely essential to the maintenance of life."

Watch the video -- Rabbi Sacks provides an important lesson not only in science and philosophy but in the human art of treating an opponent with unfailing grace, warmth, and a genuine friendliness that can't be faked and that disarms even Richard Dawkins.

On the junk DNA point, though, Dawkins manages to squirm out and seems to turn it to his own advantage (at about 13:00). In his telling now, the discovery that junk DNA is not junk at all isn't a blow to Darwinist predictions but -- yes, you guessed right -- exactly what a Darwinist would expect.

I have noticed that there are some creationists who are jumping on [the ENCODE results] because they think that's awkward for Darwinism. Quite the contrary it's exactly what a Darwinist would hope for, to find usefulness in the living world....

Whereas we thought that only a minority of the genome was doing something, namely that minority which actually codes for protein, and now we find that actually the majority of it is doing something. What it's doing is calling into action the protein-coding genes. So you can think of the protein-coding genes as being sort of the toolbox of subroutines which is pretty much common to all mammals -- mice and men have the same number, roughly speaking, of protein-coding genes and that's always been a bit of a blow to self-esteem of humanity. But the point is that that was just the subroutines that are called into being; the program that's calling them into action is the rest [of the genome] which had previously been written off as junk.

If I had been whispering at Rabbi Sacks's elbow, I would have suggested he point out that Dawkins has changed his tune. Back in 2009, in The Greatest Show on Earth (pp. 332-333), he was presenting the supposed junkiness of the vast majority of the genome as an assured scientific reality and one that is, in the specific case of "pseudogenes," "useful for. . . embarrassing creationists."

It stretches even their creative ingenuity to make a convincing reason why an intelligent designer should have created a pseudogene -- a gene that does absolutely nothing and gives every appearance of being a superannuated version of a gene that used to do something -- unless he was deliberately setting out to fool us.

Dawkins goes on:

Leaving pseudogenes aside, it is a remarkable fact that the greater part (95 percent in the case of humans) of the genome might as well not be there, for all the difference it makes.

That was in 2009, just three years ago. Back then, the purported fact that 95 percent of the human genome "might as well not be there" was an embarrassment "for creationists," whom in typical Darwinian fashion Dawkins conveniently conflates with intelligent-design advocates. Junk DNA is just what a Darwinist would expect, in other words.

Cut to 2012, and now the evident fact that "junk DNA" isn't junk at all but is instead vital for life has become "exactly what a Darwinist would hope for," namely, "to find usefulness in the living world." That is, heads you lose, tails I win. A wonderful man like Rabbi Sacks would probably have to shed his courtliness for a moment to properly call out Dawkins on this blatant, unacknowledged and suspiciously convenient self-contradiction. Ah well, as we knew already, being a Darwinist means never having to say "I was wrong." 

- See more at: http://www.evolutionnews.org/2012/09/in_debate_brita_1064521.html#sthash.DOkSSanD.dpuf

In Touchstone, Luskin Dismantles Giberson and Collins

Evolution News & Views October 10, 2012 

Don't miss Casey Luskin's gentle but nonetheless devastating dismantling of The Language of Science and Faith: Straight Answers to Genuine Questions, by Karl W. Giberson and Francis S. Collins. Writing in the current issue of Touchstone magazine, ENV's Luskin explains why the pair of authors have failed to make a persuasive case, aimed at Christians, for theistic evolution.

The basic problem is that their scientific argument is so badly outdated:

The authors' main scientific argument for neo-Darwinism is based on the existence of "pseudogenes," which they call "broken" DNA (p. 49). In their view, it is "not remotely plausible" that "God inserted a piece of broken DNA into our genomes" (p. 49). Therefore, the existence of pseudogenes "has established conclusively that the data fits a model of evolution from a common ancestor" (p. 43).

But there's a serious problem with this argument. As pro-ID biologist Jonathan Wells explains in his book The Myth of Junk DNA, scientists have discovered many examples of pseudogenes that are not "broken" but, on the contrary, perform important functions in the cell. A 2011 article by Ryan Charles Pink, et al., in the journal RNA (vol. 17, p. 792) also notes that while "pseudogenes have long been labeled as 'junk' DNA . . . recent results are challenging this moniker." The paper goes on to say, for instance, that "many pseudogenes are transcribed into RNA" and "harbor the potential to regulate their protein-coding cousins." Likewise, a 2003 paper by Evgeniy S. Balakirev and Francisco J. Ayala in the Annual Review of Genetics (vol. 37, p. 123) states that "pseudogenes that have been suitably investigated often exhibit functional roles."

Thus, if history is our guide, Giberson and Collins are likely to find their argument for "broken" DNA overturned by future discoveries.

Not too far in the future, however. Casey was writing that shortly before the release of the ENCODE results. More:

Another of their main arguments for evolution has already been challenged by mainstream science. Collins and Giberson maintain that the creative power of mutations is revealed by the evolution of "feathers from scales." (p. 38) The classical evolutionary model of feather origins did claim that feathers evolved when reptilian scales mutated to become frayed, eventually giving some advantage for flight.

But that model was abandoned when biologists discovered the great differences between feathers and scales: feathers develop as hollow tubes that grow out of special follicles in the skin, whereas scales are flat, folded skin which develop quite differently. The cover story in the March 2003 issue of Scientific American states outright that difficulties with the scale hypothesis show that the "long-cherished view of how and why feathers evolved has now been overturned." Its authors, two leading evolutionary biologists named Richard Prum and Alan Brush, further admit:

Although evolutionary theory provides a robust explanation for the appearance of minor variations in the size and shape of creatures and their component parts, it does not yet give as much guidance for understanding the emergence of entirely new structures, including digits, limbs, eyes and feathers. ("Which came first, the feather or the bird?", p. 86)

Read the rest here.

- See more at: http://www.evolutionnews.org/2012/10/in_touchstone_l_1065051.html#sthash.sRqQs5rZ.dpuf

From the Cambrian Explosion: Complex Brains and Other "Headaches" for Darwinian Evolutionists

Casey Luskin October 11, 2012 

Time to call in the media coaches, because two news stories at Science Daily show evolutionary biologists discussing difficulties posed by the Cambrian explosion. One article, "Marine Worms Reveal the Deepest Evolutionary Patterns," offers University of Bath evolutionary biologist Matthew Wills explaining the "real headache" that the Cambrian explosion causes him:

The fossils from the Cambrian period can cause a real headache for evolutionary biologists. Instinct tells us to expect simple organisms evolving over time to become increasingly more complex. However during the Cambrian period there was an apparent explosion of different major groups of animals, all appearing simultaneously in the fossil record. We looked at priapulid worms, which were among the first ever predators. What's remarkable is that they had already evolved into a diverse array of forms -- comparable to the morphological variety of their living cousins -- when we first encounter them in the Cambrian fossil record. It's precisely this apparent explosion of anatomical diversity that vexed Darwin and famously attracted the attention of Harvard biologist Stephen Jay Gould.

In the same article, biologist Marcello Ruta of the University of Lincoln confirms that one can't appeal to the incompleteness of the fossil record to explain the abrupt appearance of these worms in the Cambrian explosion:

Our work has shown that despite many new fossil finds, including many from China in the last decade, the picture remains largely unchanged. This is really important because the fossil record is notoriously incomplete. It is often difficult to know whether a pattern is just an artifact of this incompleteness, or biologically meaningful. Our study resolutely confirms the latter. Priapulids are fascinating animals with much potential in evolutionary studies. They have a long history, with the earliest known species being 505 million years old, and with some of their extinct relatives being even older. They were important components of ancient bottom-dwelling marine invertebrate communities, and their predatory habits are well documented in the fossil record. However, for all their abundance and diversity, priapulids are a remarkable and often cited example of a morphologically conservative group, their overall shape and proportions having changed relatively little during their history.

To see how little priapulids have changed since the Cambrian, compare this living priapulid worm with a couple of photographs of fossil priapulid worms from the Cambrian explosion:

Living Priapulid:

Credit: Wikipedia

Fossil Priapulid Worms from the Cambrian Explosion:

Credit: Casey Luskin

I took the lower two photographs while on a guided hike this past summer to the Burgess Shale in British Columbia, Canada. The priapulid species is Ottoia prolifica, so named because they are very common in the Burgess Shale. You can see how the priapulid body plan has essentially not changed from 505 million years ago to the present. And yet, as Wills observes, they appear in an "apparent explosion of different major groups of animals, all appearing simultaneously in the fossil record."

But this isn't the only recent story where the Cambrian explosion is seen causing headaches for evolutionary biologists. Another Science Daily article, "Cambrian Fossil Pushes Back Evolution of Complex Brains," reports on a study of the brain of a "remarkably well-preserved fossil of an extinct arthropod" named Fuxianhuia protensa, which "shows that anatomically complex brains evolved earlier than previously thought and have changed little over the course of evolution." One scientist involved in the study is quoted as stating: "No one expected such an advanced brain would have evolved so early in the history of multicellular animals." Other comments cited in the story, which summarizes a paper in Nature, strike a similar note:

• "No one expected such an advanced brain would have evolved so early in the history of multicellular animals."
• "It is remarkable how constant the ground pattern of the nervous system has remained for probably more than 550 million years."
• "The basic organization of the computational circuitry that deals, say, with smelling, appears to be the same as the one that deals with vision, or mechanical sensation."
• "In principle, Fuxianhuia's is a very modern brain in an ancient animal."

The Nature paper, "Complex brain and optic lobes in an early Cambrian arthropod," likewise states:

The early origin of sophisticated brains provides a probable driver for versatile visual behaviors, a view that accords with compound eyes from the early Cambrian that were, in size and resolution, equal to those of modern insects and malacostracans.

In other words, highly complex brains appeared early in the Cambrian explosion, without evolutionary precursors. What a headache!

Cover-story image: Burgess Shale, south end of the quarry; photo by Casey Luskin.

- See more at: http://www.evolutionnews.org/2012/10/from_the_cambri_1065181.html#sthash.CJfY05n7.dpuf

Dover Revisited: With Beta-Globin Pseudogene Now Found to Be Functional, an Icon of the "Junk DNA" Argument Bites the Dust

Casey Luskin April 23, 2013

A new paper in Genome Biology and Evolution argues that the famous beta-globin pseudogene is functional. Why is this pseudogene famous?

Well, it's been Exhibit A -- literally, offered as evidence in a court case -- for critics of intelligent design who argue that our genome is full of useless, functionless junk, and therefore can't be a product of design. Near the beginning of his testimony on the very first day of the 2005 Kitzmiller v. Dover trial, Brown University biology professor Kenneth Miller testified to the court that the beta-globin pseudogene is "broken, and it has a series of molecular errors that render the gene non-functional." (Day 1 AM, p. 79.) He further told the court:

And the fact that all three of these species have matching mistakes leads us to just one conclusion, and that's the same conclusion that Charles Darwin predicted almost a century and a half ago, and that is that these three species share a common ancestor. Matching mistakes are evidence of common ancestry. (Day 1 AM, p. 81)

In his 2008 book Only a Theory, Miller is even more explicit in asserting that this pseudogene refutes intelligent design. He writes that "A detailed analysis of the beta-globin pseudogene shows a series of mutations have rendered it nonfunctional" (p. 102). In Miller's view, that takes care of ID:

The gorilla and chimpanzee pseudogenes have exactly the same set of molecular errors [in their beta-globin pseudogene] ... There's no escaping the implication of these matching mistakes, and there's no point in arguing that six identical mistakes could have turned up independently in three unrelated species. The only sensible interpretation is that the original errors developed at random in a single common ancestor of these three species. In a court of genetic copyright law, any motion that a designer could claim originality for the human genome would be tossed out in a flash. (pp. 102-103)

Now a new paper in Genome Biology and Evolution, "Evolutionary Constraints in the β-Globin Cluster: The Signature of Purifying Selection at the δ-Globin (HBD) Locus and Its Role in Developmental Gene Regulation," argues that the beta-globin pseudogene is not broken, but in fact performs an important function in regulating gene expression. From the abstract:

HBD encodes the d-globin chain of the minor adult hemoglobin (HbA₂), which is assumed to be physiologically irrelevant. Paradoxically, reduced diversity levels have been reported for this gene. In this study, we sought a detailed portrait of the genetic variation within the β-globin cluster in a large human population panel from different geographic backgrounds. We resequenced the coding and noncoding regions of the two adult β-globin genes (HBD and HBB) in European and African populations, and analyzed the data from the β-globin cluster (HBE,HBG2, HBG1, HBBP1, HBD, and HBB) in 1,092 individuals representing 14 populations sequenced as part of the 1000 Genomes Project. Additionally, we assessed the diversity levels in nonhuman primates using chimpanzee sequence data provided by the PanMap Project. Comprehensive analyses, based on classic neutrality tests, empirical and haplotype-based studies, revealed that HBD and its neighbor pseudogene HBBP1 have mainly evolved under purifying selection, suggesting that their roles are essential and nonredundant. Moreover, in the light of recent studies on the chromatin conformation of the β-globin cluster, we present evidence sustaining that the strong functional constraints underlying the decreased contemporary diversity at these two regions were not driven by protein function but instead are likely due to a regulatory role in ontogenic switches of gene expression.

(Ana Moleirinho, Susana Seixas, Alexandra M. Lopes, Celeste Bento, Maria J. Prata, and Antonio Amorim, "Evolutionary Constraints in the β-Globin Cluster: The Signature of Purifying Selection at the δ-Globin (HBD) Locus and Its Role in Developmental Gene Regulation," Genome Biology and Evolution, Vol. 5(3): 559-571 (2013) (emphasis added).)

Allow me to help translate.

Humans have six genes related to producing beta-globin, a protein that is one of the two types of globin-molecules that combine to form hemoglobin. Of those six genes, five encode the beta-globin protein, but the sixth, the famous beta-globin pseudogene, has a premature stop codon that prevents it from producing a complete RNA transcript for beta-globin. Darwinian presuppositions have led many scientists, including Ken Miller, to assume this "pseudogene" was "non-functional" genetic junk. However, some researchers were willing to think independently and dig a little deeper.

The researchers in this study looked at copies of the beta-globin genes (including the pseudogene copy, named HBBP1) from 1,092 humans, and from 14 populations around the world. They also looked at chimpanzee copies of the same genes. When they compared all these copies of the genes from different populations and species, they found that the genes, including HBBP1, the pseudogene copy, had less variation (i.e., fewer differences) than would be expected if they were non-functional and, accordingly, accumulating neutral mutations at a constant rate. This suggests that the beta-globin pseudogene is not "non-functional," and has a function.

Of course we know that the beta-globin pseudogene doesn't create a complete RNA transcript for a beta-globin protein. But that doesn't mean it can't play roles in gene expression. That's exactly what the investigators think this protein does, and thus they write: "the strong functional constraints underlying the decreased contemporary diversity at these two regions were not driven by protein function but instead are likely due to a regulatory role in ontogenic switches of gene expression."

Interestingly, they found that regions adjoining the genes exhibit high levels of variation, suggesting that the pseudogene is under "purifying selection" -- i.e., it performs a function and thus natural selection selects against mutations that would change the sequence of the pseudogene:

Taken together, the results obtained for the β-globin cluster cannot be reconciled with other explanatory hypotheses rather than purifying selection: the low values of nucleotide diversity are confined to HBD and HBBP1 and do not extend into the flanking regions which display contrastingly high levels of variation; the haplotype structure of HBD and HBBP1 are similar across worldwide populations

So what is the function? They write: "These recent findings suggest that HBD and HBBP1 might be involved in chromatin looping in the human β-globin cluster, a crucial mechanism for temporal coordination of gene expression." Specifically, they think HBD and HBBP1 play a crucial role in regulating gene expression during development: "we propose that the complex patterns of diversity observed in this genomic region arose from distinct functional constraints related with the intricate process of chromatin and protein interactions coordinating the differential expression of genes at the β-globin cluster during development" (emphasis added).

Of course more work will have to be done to identify the details of exactly how this pseudogene works to regulate gene expression, but given that other studies have already found that chromatin looping is involved in regulating expression of globin genes, the proposal in this paper appears sound. Indeed another recent paper in Genome Research found that the HBBP1 beta-globin pseudogene is associated with DNase I hypersensitivity, which means it is transcribed, and potentially functional. The bottom line is that whatever the exact mechanism turns out to be, it seems strongly supported now to say that this "pseudogene" has genuine function.

But Ken Miller's argument for Darwinian evolution, and against ID, depends on the beta-globin pseudogene being "non-functional," implying as he does that the genetic differences between it and protein-coding beta-globin genes are errors. In light of this new evidence for the functionality of the beta-globin pseudogene, it seems that those genetic differences may not be errors at all. If so, then Miller's argument, his Exhibit A, collapses.

Image: Ronald Reagan Federal Building and Courthouse, Harrisburg, PA/Wikicommons.

- See more at: http://www.evolutionnews.org/2013/04/an_icon_of_the_071421.html#sthash.kPWaMSuI.uMmxWQar.dpuf

Proteins and Genes, Singletons and Species
Branko Kozulić
Gentius Ltd, Petra Kasandrića 6, 23000 Zadar, Croatia






Abstract

http://vixra.org/pdf/1105.0025v1.pdf

Some testable predictions entailed by Dr. Kozulic’s model of Intelligent Design

May 9, 2013

Posted by vjtorley

In my last post, The Edge of Evolution?”, I drew readers’ attention to a 2011 paper by the Croatian biochemist Dr. Branko Kozulic, titled, Proteins and Genes, Singletons and Species, which argues that the presence of not one but literallyhundreds of chemically unique proteins in each species is an event beyond the reach of chance, and that since these proteins exhibit specified complexity (as the amino acids which make up the polypeptide chain need to be in the correct order), each species must therefore be the result of intelligent planning. (A parallel argument can be made for de novo protein-coding genes.)

In this short post, I’d like to discuss a few falsifiable predictions which I believe are entailed by Dr. Kozulic’s hypothesis that Intelligent Design in Nature extends right down to the level of the species, in conjunction with his proposal that theconcept of a species, which is defined in various ways in the field of biology, can best be defined in terms of the unique proteins and genes that characterize each species.

On a general level, the predictions made by Dr. Kozulic’s Intelligent Design model can be summed up in the following two propositions:

1. If two populations of organisms are known to share a common ancestry, and to have diverged from one another relatively recently, as a result of either unguidednatural processes or human artificial selection, then there should not be any proteins or protein-coding genes that are unique to one of the two populations. (According to Dr. Kozulic’s Intelligent Design model, unguided processes are incapable of creating the hundreds of unique proteins and genes that characterize each species, within the time available; and of course, humans can’t accomplish this feat by selective breeding, either.)

2. If two populations of organisms are identified by biologists as distinct specieson the basis of several independent criteria, then there should always be some proteins and protein-coding genes that are unique to each population. (According to Dr. Kozulic’s Intelligent Design model, each species of living organism can be characterized by proteins and genes that are unique to it.)

Falsification of proposition 1 would be absolutely fatal for Dr. Kozulic’s model of Intelligent Design. At the very least, it would mean that neither proteins nor protein-coding genes could be used to define the concept of a species, as he suggests. More importantly, it would also seem to imply that new proteins and protein-coding genes can originate as a result of unguided natural processes. (One might try to argue that perhaps the proteins and genes were originally present in both populations, but that some proteins and genes were subsequently lost from one population, but in my view, such an argument would be highly implausible. How could a population of organisms lose hundreds of proteins, as well as the genes that code for them?)

Falsification of proposition 2 would not be so serious: all it would mean is that the edge of evolution does not lie at the level of the species, as Dr. Kozulic hypothesizes, but at a higher taxonomic level – say, that of the genus. That should cause no alarm to Intelligent Design proponents, including those who profess to be old- or young-earth creationists. (Creationists entertain a wide variety of views as to what constitutes a “created kind”.)

Using Proposition 1, we can make the following predictions:

(a) If there are any genuine cases of ring species – and I say if because there are only four such species known in Nature, and some of the classic examples of ring species have recently been thrown into doubt – then there should be no proteins or genes which are unique to one population within that species;

(b) Domesticated animals should have the same proteins and protein-coding genes as their wild counterparts. For example, the domestic dog and its sole ancestor, the gray wolf (pictured above, courtesy of Wikipedia), should have the same proteins and genes.

(c) Man-made hybrid species, such as the mule, should not possess any proteins or protein-coding genes which are unique to that species.

Proposition 2 implies that any two species which are agreed by biologists to be genuinely distinct from one another should each possess (hundreds of) unique proteins and protein-coding genes.

The one case that I’d really like to see Intelligent Design biologists investigate is cichlid fish: a large family comprising up to 3,000 species, which are thought to have diverged within the last 10 million years. However, some of these species diverged much more recently, within the last few thousand years, making it very likely that their diversification was an unguided natural event. The question scientists need to examine is: which of these species possess unique proteins and protein-coding genes?

The following abstract by Barluenga et al. (“Sympatric speciation in Nicaraguan crater lake cichlid fish”, Nature, 2006 Feb 9; 439(7077): 719-723) illustrates what I’m getting at:

Sympatric speciation, the formation of species in the absence of geographical barriers, remains one of the most contentious concepts in evolutionary biology. Although speciation under sympatric conditions seems theoretically possible, empirical studies are scarce and only a few credible examples of sympatric speciation exist. Here we present a convincing case of sympatric speciation in the Midas cichlid species complex (Amphilophus sp.) in a young and small volcanic crater lake in Nicaragua. Our study includes phylogeographic, population-genetic (based on mitochondrial DNA, microsatellites and amplified fragment length polymorphisms), morphometric and ecological analyses. We find, first, that crater Lake Apoyo was seeded only once by the ancestral high-bodied benthic species Amphilophus citrinellus, the most common cichlid species in the area; second, that a new elongated limnetic species (Amphilophus zaliosus) evolved in Lake Apoyo from the ancestral species (A. citrinellus) within less than approximately 10,000 yr; third, that the two species in Lake Apoyo are reproductively isolated; and fourth, that the two species are eco-morphologically distinct.

If the two species Amphilophus citrinellus (pictured above, courtesy of Wikipedia and Omnitarian) and Amphilophus zaliosus are not only reproductively isolated but also eco-morphologically distinct, then we have multiple independent grounds for regarding them as bona fide species. In that case, Dr. Kozulic’s Intelligent Design model would predict that these species should each possess their own unique proteins and protein-coding genes. And if this turns out to be the case, then Kozulic’s model would imply that the daughter species did not arise as a result of ordinary natural processes, but as a result of intelligent manipulation of the ancestral species’ genome, less than 10,000 years ago. Obviously, there is a lot of research that needs to be done in this area.

Finally, I’d like to close with a brief discussion of Neanderthal man (depicted above, courtesy of UNiesert and Wikipedia), who is believed to have diverged from Homo sapiens somewhere between 350,000 and 700,000 years ago (when their presumed common ancestor, Heidelberg man, lived), but who is also thought to have interbred with modern human beings between 80,000 and 50,000 years ago, in Eurasia. (The skeleton of what is believed to have been a Neanderthal-Homo sapiens hybrid was found recently in Italy.) Neanderthal genes make up as much as 1 to 4% of the genome of Europeans living today. Despite his ability to inter-breed with modern man, many authorities classify Neanderthal man as a separate species, Homo neanderthalensis; however, others prefer to classify him as a subspecies, Homo sapiens neanderthalensis, placing modern man in the subspecies Homo sapiens sapiens. The ability to inter-breed does not necessarily indicate that Neanderthal man was the same species as we are; apparently, there are documented cases of two species hybridizing and producing fertile offspring and also of gene flow from one species into the gene pool of another by the repeated backcrossing of an interspecific hybrid with one of its parent species, so evidence of inter-breeding does not necessarily indicate that Neanderthal man was of the same species as we are.

Neanderthals had a brain the size of ours and are believed to have had a language, and they seem to have buried their dead with flowers, grave goods and ocher, although this remains controversial. On the other hand, the marked lack of innovation in their tool-making and the absence of conclusive evidence that Neanderthals created anything symbolic has led anthropologist Ian Tattersall, of the American Museum of Natural History, to doubt that they possessed the mental capacities that distinguish modern humans from other animals: “Burial in the simple Neanderthal style falls short of furnishing us with convincing proof of symbolic activity among these extinct hominids”, he declared in a recent interview. (Tattersall’s article, An Evolutionary Framework for the Acquisition of Symbolic Cognition by Homo sapiens, in Comparative Cognition and Behavior Reviews, 2008, Volume 3, pp 99-114, is also well worth reading.)

The question of whether Neanderthal man possessed unique proteins and genes is therefore one of vital importance for understanding who we are, and who this ancient human really was. As far as I can tell, he did possess a few unique genes. More information about Neanderthal genes can be found here, here, here andhere. According to the study, A Draft Sequence of the Neandertal Genome by R. Green, D. Reich, S. Paabo et al. (Science, 7 May 2010: Vol. 328 no. 5979 pp. 710-722, DOI: 10.1126/science.1188021):

Features that occur in all present-day humans (i.e., have been fixed), although they were absent or variable in Neandertals, are of special interest. We found 78 nucleotide substitutions that change the protein-coding capacity of genes where modern humans are fixed for a derived state and where Neandertals carry the ancestral (chimpanzee-like) state (Table 2 and table S28). Thus, relatively few amino acid changes have become fixed in the last few hundred thousand years of human evolution; an observation consistent with a complementary study (57). We found only five genes with more than one fixed substitution changing the primary structure of the encoded proteins. One of these is SPAG17, which encodes a protein important for the axoneme, a structure responsible for the beating of the sperm flagellum (58). The second is PCD16, which encodes fibroblast cadherin-1, a calcium-dependent cell-cell adhesion molecule that may be involved in wound healing (59). The third is TTF1, a transcription termination factor that regulates ribosomal gene transcription (60). The fourth is CAN15, which encodes a protein of unknown function. The fifth is RPTN, which encodes repetin, an extracellular epidermal matrix protein (61) that is expressed in the epidermis and at high levels in eccrine sweat glands, the inner sheaths of hair roots, and the filiform papilli of the tongue.

For those readers who (like myself) dislike jargon, here’s a less technical summary by the Smithsonian National Museum of Natural History (Ancient DNA and Neanderthals, page 3):

Researchers found 78 sequence differences that would have affected proteins in which Neanderthals had the ancestral state and modern humans had a newer, derived state. Five genes had more than one sequence change that affected the protein structure. These proteins include SPAG17, which is involved in the movement of sperm, PCD16, which may be involved in wound healing, TTF1, which is involved in ribosomal gene transcription, and RPTN, which is found in the skin, hair and sweat glands. Scientists do not know the function of the CAN15 protein, which was also one of the differences. Other changes may affect regulatory regions in the human sequence. Some changes are in regions that code for microRNA molecules that regulate protein manufacture.

As far as I can tell (and I’m not a scientist), most of the differences referred to above would have involved modifications in existing proteins, rather than brand new ones appearing, although apparently Neanderthals were missing the protein repetin, making them better adapted to the cold, but less so to disease. However, one swallow does not make a summer, and geneticist Jeff Tomkins writes: “Modern humans and Neanderthals are essentially genetically identical.” It seems, then, that on Dr. Kozulic’s Intelligent Design model, modern humans and Neanderthals constitute a single species, which means that their divergence could have occurred as a result of ordinary natural processes.

Before I finish, I’d like to thank bornagain77 for having alerted me to the existence of ‘species specific’ alternative splicing codes, which are described in an article entitled, Evolution by Splicing by Ruth Williams (The Scientist, December 20, 2012):

A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?” said Ben Blencowe, a cell and molecular biology professor at the University of Toronto, who led one of the studies. A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge, biology and biological engineering professor at Massachusetts Institute of Technology and lead author of the second paper, found that gene expression is relatively conserved among species.

On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe. “Alternative splicing is evolving faster than gene expression,” concluded Tom Cooper, professor of pathology at Baylor College of Medicine in Houston, Texas, who was not involved in the work.

It would be interesting to see if alternative splicing patterns “carve up” species of organisms in the same way as Dr. Kozulic’s proposed method of using unique proteins and protein-coding genes as defining characteristics of species.

I shall stop here and throw the discussion open to readers. Can anyone think of some other testable predictions of Dr. Kozulic’s model of Intelligent Design? Over to you.

http://www.uncommondescent.com/intelligent-design/some-testable-predictions-entailed-by-dr-kozulics-model-of-intelligent-design/

Sorry, Ring Species Do Not Provide Good Evidence for the Origin of New Species by the Darwinian Mechanism

Evolution News & Views April 6, 2012

Before Darwin, fossils had already provided good evidence that new species have arisen at many times in the history of life. In 1859, Darwin proposed that new species originate when populations of an existing species diverge over time through the natural selection of small variations. (In the modern version of his theory, new variations are supplied by genetic mutations.) Although Darwin had no evidence for natural selection, it has since been documented in the wild. Nevertheless, biologists have never actually observed the origin of a new species by variation and selection.

In the absence of direct observation, indirect evidence is used to support Darwin's theory. Ring species are a widely cited example of such indirect evidence. Ring species are chains of geographically adjacent populations, in which each population interbreeds freely within itself but somewhat less freely with those adjacent to it, and the populations at the ends of the chain do not interbreed when they come in contact. By the most common definition of "species," the populations at the ends of the chain have become separate species.

If a ring species existed it would not be an example of observed speciation, because the chain would already be in place. But a ring species would provide good indirect evidence that speciation can occur as Darwin proposed, with populations diverging gradually in different environments until their descendants can no longer interbreed.

The classic example of a ring species was the herring gull, with populations circling the northern hemisphere. But this example is not what it has been advertised to be. In a 2004 paper titled "The herring gull complex is not a ring species," German and Dutch biologists concluded:

What earlier authors... regarded as "the herring gull" turned out to be an assemblage of several distinct taxa (argentatus, vegae, smithsonianus), which are not each other's closest relatives. Our results show that the ring-species model does not adequately describe the evolution of the herring gull group.

Another often cited example was the Ensatina salamander. Populations of this animal circle the mountains around California's Central Valley. Like the herring gull example, the salamander example is not what it has been advertised to be, but for the opposite reason. Whereas the birds in the first example turned out to be separate species that are not closely related, the salamanders turn out to be members of the same species, Ensatina eschscholtzii. The populations at the ends of the chain are varieties that interbreed to a limited extent. In 1997, Berkeley salamander expert David Wake concluded that "the complex appears to be in a state of incipient species formation."

Now, "incipient species" is a term that was introduced by Darwin to mean varieties that are predicted to become separate species in the future. And if they do, that would constitute evidence for the origin of new species by a Darwinian mechanism. But what if they don't go on to form separate species? What if, like the Galápagos finches, they go the other way and start forming hybrids that are hardier than the parents -- that is, they merge rather than diverge?

Calling two populations "incipient species" is not empirical evidence, but a theoretical prediction.

None of this has much bearing on intelligent design. The two salamander populations at the ends of the California chain are not distinguished by features that would have to be produced by an intelligent agent. The issue is not ID, but whether the evidence supports Darwin's theory as much as his followers claim it does.

Photo credit: Herring Gull at Fuglsang Beach, the northern part of Funen, Denmark; Malene Thyssen/Wikicommons.

- See more at: http://www.evolutionnews.org/2012/04/sorry_ring_spec058261.html#sthash.cYS7WVBw.dpuf