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Human/Ape Common Ancestry: Following the Evidence

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Human/ape common ancestry has been a subject much discussed recently. A friend wrote me asking for links dealing with human/ape common ancestry. While there are numerous good articles that have talked about this issue from an intelligent design (ID) friendly perspective, I tried to provide him with some helpful links and information.

As a preliminary point, it's important to note that human/ape common ancestry is compatible with ID. Nonetheless, ID proponents are interested in taking a scientific approach to these questions, and the evidence suggests that even modest changes requiring two or more mutations before conferring any adaptive benefit could not arise via Darwinian evolution under any reasonable timescale involving human/ape common ancestry. As a result, questions about human/ape common ancestry should be on the table for people who really want to follow the evidence where it leads.

The basic issue is this: Despite the fact that human/ape genetic similarities are often overstated, YES, in many instances it is true that humans and chimps have very high levels of genetic similarity. Does this functional genetic similarity bolster neo-Darwinian evolution and human/ape common ancestry? Not at all. In fact, we could have predicted these similarities without any knowledge of Darwinian evolution simply by observing that humans have similar body plans to apes. If similar morphology implies similar genetics, then we could predict these high levels of similarities without even thinking about considerations pertaining to common ancestry.

But there's another important point to consider: Functional morphological and genetic similarities between humans and apes could be the result of common design just as much as common descent. That's a good principle to keep in mind as you investigate this issue: functional biological similarity is explained by common design just as well as it's explained by common descent. (In fact, in some cases--such as extreme convergent evolution--such similarity is explained much better by common design.)

There are a lot of good articles out there on this topic, but here is a summary of some articles germane to recent debates:

(1) Casey Luskin and Logan Paul Gage, "A Reply to Francis Collins' Darwinian Arguments for Common Ancestry of Apes and Humans," in Intelligent Design 101: Leading Experts Explain the Key Issues, edited by H. Wayne House (Kregel, 2008), provides a rebuttal to many of Collins' arguments for human/ape common ancestry:

a. This article notes that the evidence for human chromosomal fusion simply shows that our human lineage underwent a fusion event and doesn't say anything about whether our lineage shares a common ancestor with apes. For another good article on problems with the telomeric evidence for human chromosomal fusion, see "Guy Walks Into a Bar and Thinks He's a Chimpanzee: The Unbearable Lightness of Chimp-Human Genome Similarity."

b. Collins cites much "junk DNA" as alleged evidence of our shared ancestry with apes, but this DNA turns out to NOT be junk at all.

c. Collins makes weak arguments that a couple mutation in a gene could have produced human cognition--this is an outlandish hypothesis that is easily rebutted.

d. For another recent rebuttal to Collins on the issue of junk DNA and human/ape common ancestry, please see "Francis Collins' Junk DNA Arguments Pushed Into Increasingly Small Gaps in Scientific Knowledge.

e. For background on functions for pseudogenes, see "Et tu, Pseudogenes? Another Type of 'Junk' DNA Betrays Darwinian Predictions".

(2) "Human Origins and Intelligent Design," Progress in Complexity, Information, and Design, Vol. 4.1 (July, 2005).
a. This article reviews the fossil evidence for human/ape common ancestry and finds that it is lacking.

b. There is also a less-technical version of this article here.

(3) "The myth of 1% human-chimp genetic differences"
a. This article asks whether human/chimp genetic similarities are good evidence for common ancestry. As the journal Science has reported, it notes that human/chimp genetic differences are much more than the "1%" genetic difference we typically hear about.

b. This article also notes that human/ape genetic similarities might result from common design rather than common descent.

c. This piece asks what is the metric for demonstrating Darwinian evolution based upon genetic similarity. There doesn't seem to be one, and the argument often appears arbitrary.

d. In fact there are some parts of our genome, such as the human y chromosome, that are radically different from the chimp genome. For details, see: "Recent Genetic Research Shows Chimps More Distant From Humans, Neanderthals Closer."

e. Geneticist Richard Buggs has an excellent article which argues that the degree of similarity between the human and chimp genome might be as low as 70%:

To compare the two [human and chimpanzee] genomes, the first thing we must do is to line up the parts of each genome that are similar. When we do this alignment, we discover that only 2400 million of the human genome's 3164.7 million 'letters' align with the chimpanzee genome - that is, 76% of the human genome. Some scientists have argued that the 24% of the human genome that does not line up with the chimpanzee genome is useless "junk DNA". However, it now seems that this DNA could contain over 600 protein-coding genes, and also code for functional RNA molecules.

Looking closely at the chimpanzee-like 76% of the human genome, we find that to make an exact alignment, we often have to introduce artificial gaps in either the human or the chimp genome. These gaps give another 3% difference. So now we have a 73% similarity between the two genomes.

In the neatly aligned sequences we now find another form of difference, where a single 'letter' is different between the human and chimp genomes. These provide another 1.23% difference between the two genomes. Thus, the percentage difference is now at around 72%.

We also find places where two pieces of human genome align with only one piece of chimp genome, or two pieces of chimp genome align with one piece of human genome. This "copy number variation" causes another 2.7% difference between the two species. Therefore the total similarity of the genomes could be below 70%.

Be sure to also read Dr. Buggs' follow-up article that answers questions and objections about his argument.

(4) "Study Reports a Whopping '23% of Our Genome' Contradicts Standard Human-Ape Evolutionary Phylogeny"
a. This article shows how the genetic data is actually painting a very confusing picture about human common ancestry with apes.

b. The paper reports: "For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee."

c. Another article which elaborates on similar problems is at "Primate Phylogenetics Researchers Swinging from Tree to Tree."

d. Likewise, Jonathan M. recently reported that ERV distributions conflict with the standard phylogeny of human/ape relationships.

(5) In the past few years quite a bit has been written on challenges to widely touted "missing links." Rebuttals can be found in articles like:
a. Lucy: "My Pilgrimage to Lucy's Holy Relics Fails to Inspire Faith in Darwinism."

b. Ardi: "The Overselling of Ardipithecus ramidus."

c. Ida: "The Rise and Fall of Missing Link Superstar 'Ida'."

d. Neanderthals: For a discussion of why Neanderthals don't show anything like human/ape common ancestry, please see: "Does Giberson and Collins' Neanderthal Argument Demonstrate 'Common Ancestry'?"


26 Comments

Dear Dr. Matheson,

Thank you for your kind reply. Let me say that I appreciate that you say that we are not “enemies”—on that point I could not agree with you more, and if you ever want to have lunch, I would be grateful for the opportunity. I’m not sure if I’ll be in Michigan anytime soon, but if you make it out to the Seattle area, please let me know and I’d love to take you to lunch. I’m sure it would be a fruitful conversation.

As an initial point, I don’t think that my claim was a ”falsehood”—it was simply not completely clear, and in the absence of clarity one should ask for clarification and not presume the “falsehood” interpretation. You kindly accepted my clarification as an accurate one—and one which was completely consistent with everything I’d been writing—and we both agree that once clarified my point was not a “falsehood.” So I think “falsehood” is an unfair allegation.

Regarding (1), I really appreciate your clarification here and I now sense we are talking about 2 very different meanings of “intelligent design.”

From your perspective, as long as there’s an omnipotent God lurking somewhere in the background, then God can guide the evolutionary process such that it appears to be unguided. You view this as a form of ‘intelligent design,’ that is unfalsifiable. But I would not call this ‘intelligent design’ but rather I would call this ‘deistic design,’ where the design is present but undetectable (and not falsifiable). Such deistic design is quite different from what is postulated by the scientific theory of intelligent design, which postulates, by definition, design which is detectable. In that regard, if you redefine ‘intelligent design’ as ‘potentially undetectable and unfalsifiable design’ then that’s not what I’m talking about. What I’m talking about is called the scientific theory of intelligent design.

I sense that your attack on ID might unfairly put ID in a catch-22 situation:

(a) If ID does NOT detect deistic design, then ID is bad theology by claiming God can’t use material causes.
(b) If ID DOES detect deistic design then ID is bad science because then it is denying material causes in instances where material causes are clearly the best explanation. Moreover, in this case you would say ID is unfalsifible because it detects design in all instances.

If you can forgive the double-negatives, here is my thesis: both claims (a) and (b) misunderstand ID, and ID is not bad theology, nor is it bad science. Please let me explain:

Regarding (a), ID in fact does not claim to detect ‘deistic design’ where an omnipotent God is lurking in the background, using wholly material causes to create life. Thus ID is not unfalsifiable since it doesn't apply in all instances. At the same time, ID doesn’t make for bad theology since ID proponents don’t deny that God can use secondary material causes to achieve His will—e.g. ‘deistic design’. In those instances ID would say that material causes are the best explanation.

In fact, since ID is a scientific theory, it doesn’t purport to investigate such scientifically untestable theological questions about whether God is out there guiding the evolutionary process such that it appears unguided. You can’t attack ID for this because this makes ID identically situated to evolutionary biology, which doesn’t claim that there is no God out there overseeing the evolutionary process.

Regarding (b), ID doesn’t claim to detect deistic design--again, it is not unfalsfiable since it doesn't purport to detect design in all instances.

Scientifically, ID agrees that when material causes are the best explanation for an observed phenomenon, then we should go with that material explanation. So if deistic design is at work, ID will detect material causes. Please let me elaborate:

Let’s say that human intelligent agents plant flowers that spell “Welcome to Disneyland.” Here, the theory of ID would detect intelligent agency intervening in the natural order of how plants grow. This represents the empirically detectable action of intelligent agents. While ID proponents don’t deny that God can act in other ways, that’s all the scientific theory of ID purports to detect.

To further illustrate that last sentence, let’s say that human intelligent agents plant flowers in a random fashion that mimics what we might find on a hillside of wildflowers. Perhaps in this case the design is not detectable. But the flowers were really planted by intelligence. So ID fails to detect intelligent agency. Is this a problem? In this case, I readily admit that the scientific theory of ID might produce a false negative with regards to detecting design in some cases (i.e. it really was designed, but we’re not detecting design), especially when a designer acts in such a way as to mimic unguided material causes.

I see this not as a weakness of ID, but a strength.

The scientific theory of ID is very sensitive to wrongly inferring design, and tries to avoid false positives for ID (i.e. claiming to detect design when something wasn’t actually designed). ID is less concerned with false negatives – i.e. inferring material processes when something really was designed. Rather than being a weakness in ID, this shows the very cautious, conservative, and scientific nature of the theory of ID. In other words, the scientific theory of ID only scientifically detects design when we’re really sure that intelligent design is correct. No one can fault ID for being cautious, so again, this is a strength, not a weakness, of ID.

Thus, in closing, ID is a scientific theory and not a theological doctrine. As a scientific theory, it claims to detect design when scientifically warranted (so it doesn’t violate (b)), but it doesn’t make theological claims that if we don’t detect design then somehow God is completely absent from the process in a theological sense (so it doesn’t violate (a)). Again, ID is concerned with scientific questions, not theological ones.

ID detects intelligent design, not deistic design. So your problem with ID is based upon a misunderstanding of how the theory works: ID doesn’t claim to design is detectable in all instances, even if God was at work using deistic design. But ID does claim that design is detectable in some instances. Thus, ID makes testable claims that are limited, and is not unfalsifiable.

Regarding (2) you charge that I “have steered the conversation away from primate genomics all the way to the root of the tree of life.” (I find this charge ironic since your last comment brought in issues related to bacterial evolution which have no relevance to this conversation whatsoever.)

While I did certainly talk about aspects of the tree of life from the bottom to the top, there was an important purpose here that must be understood, because that purpose directly related to our discussion about primate genomics:

My purpose was to first make an argument first showing problems exist in constructing broad portions of the tree of life, and then second, to show those same problems exist (to a significant degree!) within the upper branches of the primate portions of the tree.

Thus, first I documented the types of problems in constructing a ‘tree of life’ which have caused some scientists to say things like:

“[t]he problem was that different genes told contradictory evolutionary stories”
“We've just annihilated the tree of life”
“the history of life cannot properly be represented as a tree”
“Phylogenetic incongruities can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves.”

The problem in each of these cases was that the data could not be placed into a nice, neat nested hiearachy. The basic problem is that functional biological similarity was constantly appearing in places NOT predicted by common descent. Thus, when you write in item (3), “Returning to the concept of explanation I used above, let me note that if you wish to falsify common descent, then you must produce data or observations that cannot be explained by common descent, in principle,” my response is this: In my view, common descent has failed to explain this data, which is precisely why in many cases evolutionary biologists are resorting to explanations like convergent evolution, horizontal gene transfer, differential allele fixation times, rapid evolution, to explain why shared biological similarities appears where it does.

Some of these ad hoc explanations may appear reasonable -- horizontal gene transfer, convergent evolution, differing rates of evolution (rapid evolution is conveniently said to muddy any phylogenetic signal), fusion of genomes -- but at the end of the day, we must call them what they are: ad hoc explanations designed to save common descent from its failure to explain why biological similarity appears in so many unexpected places.

Perhaps common descent doesn’t fail to explain the data instances (a) and (b), but if it fails to explain the distribution of biological traits in instances (c), (d), and (e), then how do we know it is working in instances (a) and (b)? Simon Conway Morris explains this problem with respect to convergent evolution, where convergent evolution is so common that it becomes very difficult to distinguish between convergence and homology that results from common inheritance:

I believe the topic of convergence is important for two main reasons. One is widely acknowledged, if as often subject to procrustean procedures of accommodation. It concerns phylogeny, with the obvious circularity of two questions: do we trust our phylogeny and thereby define convergence (which everyone does), or do we trust our characters to be convergent (for whatever reason) and define our phylogeny? As phylogeny depends on characters, the two questions are inseparable. ... Even so, no phylogeny is free of its convergences, and it is often the case that a biologist believes a phylogeny because in his or her view certain convergences would be too incredible to be true. ...

During my time in the libraries I have been particularly struck by the adjectives that accompany descriptions of evolutionary convergence. Words like, 'remarkable', 'striking', 'extraordinary', or even 'astonishing' and 'uncanny' are common place...the frequency of adjectival surprise associated with descriptions of convergence suggests there is almost a feeling of unease in these similarities. Indeed, I strongly suspect that some of these biologists sense the ghost of teleology looking over their shoulders.

(Simon Conway Morris, Life's Solution: Inevitable Humans in a Lonely Universe, pp. 127-128 (Cambridge University Press, 2003).)

Because ad hoc explanations like HGT, differential allele fixation times, whole genome fusion, rapid evolution, etc. are also used to explain why biological similarity is popping up in unexpected places, we could substitute those terms in this quote for the term “convergence” and we’d have the same problem: common descent doesn’t explain the observed distribution of traits, so evolutionary biologists have to appeal to other processes.

Those exceptions to the rule of common descent are so common that it’s reasonable to ask if they swallow the rule, and make it impossible to tell when the rule of common descent is at work. The problem is this: The failure of common descent in so many specific instances is enough (for me at least) to call it into question in many other instances.

Was this entire discussion intended to somehow distract from primate genomics? Hardly!

After establishing the kinds of phylogenetic problems that are common throughout the tree of life, I then showed that this same problem exists within primate genomics. Thus, I brought the discussion home and closed it out by citing the 2007 MBE which found that huge portions of the human genome contradict the standard primate phylogeny, and also citing the 2000 Nature article by Gura which shows conflicts in the primate tree. As I then wrote as a conclusion to that section of my comment:

So I think that both shared genetic and morphological similarities between humans and apes do not always not paint a nice, neat and clean picture of alleged human / ape relationships as you claim it does. ... So looking at the diagram, it's clear that the morphological and molecular data does not always fit with a nice, neat nested hierarchy.

So my reason for talking about problems throughout the tree of life was to establish the types of problems that systematists encounter when trying to reconstruct evolutionary relationships. Having established that class of problems, I then showed that primate systematists encounter those same types of problems.

Thus, my purpose in discussing problems in constructing non-primate portion of the tree is not because I am “less interested in primate genomics,” nor was my purpose to “driv[e] our conversation … away from the careful consideration of primate genetics and genomics.”

Rather, if you read my comment, the whole punchline of this discussion was to bring the conversation BACK to a conversation about primate genetics and genomics, and it seems very clear that my entire purpose was to show that primate systematics has many of the same problems found in other parts of the tree of life. Thus, the 2007 MBE paper claimed that “[t]he human genome is a mosaic with respect to its evolutionary history,” and Gura’s Nature paper stated: “no matter how the computer analysis was run, the molecular and morphological trees could not be made to match” and “The abstract of the pair’s paper stated provocatively that ‘existing phylogenetic hypotheses about human evolution are unlikely to be reliable’.”

Sounds like primate systematics is facing similar problems that are encountered in other parts of the tree of life.

Finally, you wrote: “despite my challenging you to show me how design accounts for these same data, you have written nothing about why and how (for example) human chromosome 2 shows evidence of ‘design.’”

Actually I thought my comments already had addressed this as J. Preston asked the same question and I answered it squarely in response to him. So I wasn’t aware this topic needed to be addressed again. In case you missed it, I’m happy to repeat my answers J. Preston’s questions:

Question 1: "What explanatory power does ID offer regarding human chromosome 2?"

I reply: About the same minimal explanatory power that common descent offer for the data we observe in human chromosome 2. Sometimes the data is just what it is and no model predicts it clearly. I would say ID predicts this data no worse than common ancestry.

Also, assuming the evidence for fusion is compelling (a claim that is weakened given the evidence I've raised in this thread), at most all it shows is that humans are descended from ancestors with 48 chromosomes. Those ancestors might have been just as human as you and me. Or they might have been very ape-like. Chromosomal fusion simply does not answer that question.

Question 2: "What potential discovery regarding the status of the fusion event could falsify ID?"

I reply: Assuming for the sake of argument that the fusion evidence could establish human/ape common ancestry (which it cannot), my article above notes that "human/ape common ancestry is compatible with ID." So there are good ways to test ID (for a discussion, please see A Positive, Testable Case for Intelligent Design), but debating human/ape common ancestry is not one of them.

Question 3: "If ID is confirmed regardless of the status of the fusion is it really that strong of an explanation in this case?"

I reply: I'm not sure if I completely understand what you are getting at here. But I’ll take a stab: The case for ID depends on evidence that is far removed from the fusion evidence, so even if human chromosome 2 is the result of a fusion event and somehow this provides evidence that humans and apes share a common ancestor, that would not refute ID. So

I'm not claiming that any model here is a "strong" explanation for what we observe in human chromosome 2, whether we're talking about ID or common descent. So I reject a premise in this question.

Also, if you look at my comment in reply to you, I stated, “the fusion evidence tells us nothing about whether our lineage leads back to a common ancestor with apes (though it does reaffirm something we already knew--that humans have similar genetics to apes).” The statement in the parenthesis means that at most what the fusion evidence does is reaffirm that humans and apes share many functional genetic similarities. In that regard, I think this cashes out as one of those examples where both common design and common descent can explain the data equally well.

In fact, the article linked in point 1 of my article above makes this very point explicit:

This evidence, however, merely confirms something we already knew: humans and chimps have a similar genetic structure. As Collins reminds us, genetic similarity does not prove common ancestry, for genetic similarity may be the result of functional requirements, in this case possibly implicating common design.

So I thought I had already addressed your “challenge.”

Regarding (3), I addressed some of this above but you suggested that data from other fields could potentially also encourage you to challenge common descent. You might feel that such data doesn’t exist, but I would respectfully disagree and argue that such data exists. For example:

Phylogeny and biogeography often disagree.
Phylogeny and paleontology often disagree.
Transitional fossils are often missing (or the "predicted" transitional fossils fall apart on closer inspection).
"Homologous" structures often have different developmental pathways or different structures often have "homologous" developmental pathways.

Regarding (4), you argue that I don’t exhibit a good grasp of evolutionary biology. It’s saddening that we have to delve into this but if you insist on repeatedly making these charges, I’ll get into this.

In your previous comments you gave 3 supposed examples where I misunderstood the science of evolutionary biology, but as I explained in my prior comments, in each case you were wrong as I understood the science perfectly well. Indeed, in one case, you accused me of failing to take note of a particular paragraph in a paper, but in fact you neglected to notice that I had quoted that paragraph in full in a prior article about that paper and explained the paper’s explanation of the data perfectly well.

Again, I’m happy to let the readers decide whether I misunderstood those papers. But your quickness to wrongly conclude I misunderstood a paper leads to me to the conclusion that you operate under a working hypothesis that I don’t understand the science. But that hypothesis is not supported. You seem so eager to charge me with misunderstanding the science that you are making inaccurate charges of inaccuracy. As we’ll continue to see, this is a common pattern in your accusations.

In your latest comment, you raise three more alleged examples where I misunderstood the science. The quality and accuracy of these examples shows just how weak your hypothesis is that I don’t understand the science.

Your first accusation links to an ID the Future interview I conducted with Doug Axe about his theoretical tests of the ability of neo-Darwinian processes to produce multimutation features (features which require multiple mutations before any benefit is conferred on the organism). You then pointed me to a blog post where you supposedly critiqued Axe’s paper. But I found no critiques of that paper on your page. Perhaps you linked to the wrong interview or the wrong blog post. I’m not sure, but either way I cannot help but notice that you identified nothing I said that was purportedly wrong.

Let’s look at the big picture of what you’re arguing here: because I did a podcast interview with a scientist about his paper, and because you wrote a blog post purportedly critiquing that paper, that therefore I don’t understand evolutionary biology? That’s absolutely preposterous. This is not an argument that I got anything wrong: You’re welcome to disagree with a paper but just because I interviewed the author of that paper and let them explain the paper doesn’t mean that I committed a “glaring error.” You haven’t identified any errors I made, but rather simply critiqued someone else, not me.

(Regarding your criticisms of the Axe/Gauger 2011 paper in the page you linked to, I find your criticisms weak: In fact I talked with Ann Gauger about this objection extensively in a version of our podcast on the paper that unfortunately had recording issues and had to be scrapped. So I understand your objection and having read the paper, found that they laid out a perfectly valid rationale for their arguments. They never claimed this was an actual evolutionary transition, just that these two enzymes are so similar that they ought to be convertible by mutation. They didn’t claim to test an actual a real-life evolutionary transition, but this is meant to be a disproof of concept of the types of conversions which are commonly said to take place. That’s exactly how I described the paper in my podcast with Gauger. Both you and Todd Wood seem to have misunderstood the paper in this regard.)

You also allege a mistake regarding the evidence for human chromosomal fusion, but this allegation also pertains to comments and arguments I never made, and also shows your working hypothesis is wrong.

The fact that I discussed discrepancies with the telomeric repeats doesn’t mean that the fusion hypothesis has no explanatory power or that there is no evidence for fusion. Again, if you read the very first link of point 1 of my article I acknowledge that:

“Human chromosome 2 has a structure similar to what one would expect if two chromosomes resembling chimpanzee chromosomes 2a and 2b were fused to one another, end to end.”

What I was talking about here is the overall structure of the chromosome—the banding patterns that are shown in figure 2 of Yunis and Prakash (1982) (a figure somewhat similar to one Francis Collins reprints in his book). You think I am unaware of this evidence or deny it. Hardly. What has actually happened is once again, you haven’t taken the time to understand my position or read my writings but rather you are so eager to find errors that you are finding them where they don’t exist.

But if you read my article, you’ll find that this evidence doesn’t bolster common descent over common design. It bolsters chromosomal fusion and human/ape genetic similarities, which can be explained equally well by common design or common descent. Thus, the fusion evidence does not bolster common descent over common design:

We accept that there is good evidence that human chromosome 2 is composed of two fused chromosomes. It seems clear that a chromosomal fusion event took place at some time in our human lineage. This evidence, however, merely confirms something we already knew: humans and chimps have a similar genetic structure. As Collins reminds us, genetic similarity does not prove common ancestry, for genetic similarity may be the result of functional requirements, in this case possibly implicating common design.13 Evidence for chromosomal fusion in humans simply indicates that, at some point within our human lineage, two chromosomes became fused. This tells us nothing about whether we share a common ancestor with apes.

If you doubt that this is my main thesis regarding fusion, consider what I said in point 1 of my article here in this post: it was the exact same thing: “This article notes that the evidence for human chromosomal fusion simply shows that our human lineage underwent a fusion event and doesn't say anything about whether our lineage shares a common ancestor with apes.”

So I never denied that chromosome 2 has some evidence of fusion. Nothing I have said contradicts the banding pattern data figure 2 of 2 of Yunis and Prakash (1982), and in fact what I have said affirms it. At the end of the day, all this shows is that humans have similar genetics to ape, and that chromosome 2 in humans was likely fused. To claim this is evidence for human/ape common ancestry over common design is to go beyond what the data can tell us.

Your final example of an alleged inaccuracy deals with my article on papers that found epistatic interactions in bacteria that had negative effects upon increasing fitness. (While you wrongly accuse me of driving the conversation away from a discussion of primate genomics, it’s pretty clear that this paper has nothing to do with primate genomics!) You admit that I might have “unintentionally” mis-stated the papers. I totally get that the papers found that rate of adaptation decreased. After all, all of the quotes that I quoted from the papers say this. That’s why I wrote “As mutations increase, bacteria faced barriers to the amount they could continue to evolve.” You took issue with once statement where I wrote the mutational interactions “caused fitness to decrease.” I did unintentionally mis-state the papers in that phrase and I’ve now fixed it. But regarding this one example where there was an actual error, you yourself admit its “unintentional” nature.

At this point, I’m confronted with a dilemma: Your words have been very polite to me in this thread Dr. Matheson and I appreciate that. I have every intention of only being polite and nice towards you as well.

However, your polite words don't change the rhetorical strategy you are using that isn't so nice. In essence, your words may be nice but your actions which are intent upon making (inaccurate!) allegations of ignorance or incompetence against me, attacking my "grasp of the sweep of evolutionary biology" doesn't feel very nice. You are now playing a game where apparently my intellectual abilities, knowledge, and perhaps even my integrity are on trial, with you as the accuser and judge, and you seek to raise alleged error after alleged error all so you can make the point that I lack “credibility as an analyst of evolutionary biology.”

The very fact that you are playing this ‘accusation game’ is unfortunate. I am not obligated to sit in your judgment, but out of humility and courtesy to you, I will turn the cheek and submit myself to your accusations: In that regard,let’s review the evidence once last time.

You raised 6 examples of alleged errors I made. In 5 of those cases, it was you who made the error and wrongly accused me of being wrong, and in many of those cases it was you who failed to appreciate, or recognize, my actual my arguments. In the 6th case (the final one discussed above) you admitted that this error might have been “unintentional” and in fact it was, especially given that I correctly stated the findings of the papers elsewhere in my article. I’ve now corrected the language in my article to fix the unintentional error.

So your examples don’t back your working hypothesis that I don’t understand evolutionary biology. I think what’s really happening is the following:

This is not the first time where you have stretched to find errors in the writings of ID proponents as a rhetorical strategy. You did the same thing in your responses to Stephen Meyer’s book Signature in the Cell. In response to your responses, I wrote:

But we need to step back for a moment: Why are we even talking about this? It’s part of Matheson rhetorical strategy, cribbed from the Panda’s-Thumb playbook: He wants readers to feel that Meyer can’t be trusted, so he tries to smear him.

I think the same thing is going on here. And in that case too, many of your accusations against Stephen Meyer turned out to be wrong.

Do you really want to continue to play this “accusation game”? It’s not a nice game to play, and out of respect for you Dr. Matheson, I don’t want to play it against you.

Your responses to Stephen Meyer contained multiple errors, but I will NOT conclude “Neither bolsters Steve Matheson’s credibility as an analyst of evolutionary biology.” I don’t go there and I would never want to go there. I want to remain civil in my response to you.

I’m not here to attack your integrity or your intellectual abilities Dr. Matheson. I have no doubt that you are pursuing what you believe is truth and that you are a very competent scientist. Even if you made some errors or I disagree with you, I will NOT attack your competence as a scientist or your knowledge of evolutionary biology. We can respectfully agree to disagree without attacking one-another’s competence.

Given that all of your accusations of misunderstandings or ignorance against me have evaporated upon analysis, I think now it is you who have a choice:

Everyone makes errors sometimes. Isn’t it better to ‘judge not’ and simply rebut the arguments of one’s opponent rather than making constant accusations of general incompetence? Let’s take a more civil approach where we just critique one-another’s arguments and not constantly allege intellectual or moral failings of our opponents.

I appreciate that you refrained from the latter here in this particular dialogue, but unfortunately you did not refrain from the former.

Your working hypothesis that I don’t understand evolutionary biology is not supported by a single example you have given, and in fact the evidence you accuse me of ignoring or misrepresenting is accurately discussed in articles I’ve written. I've taken much time to carefully document all of this in my comment replies to you.

Thus, I end this comment by repeating what I said at the end of a previous comment:

If I might humbly make a suggestion:

With all due respect Dr. Matheson, you will never fully appreciate ID arguments if you constantly assume (and accuse) that we simply don’t understand the papers we’re writing about.

Nobody is perfect—myself very much included here—but generally speaking we do understand the papers we’re writing about. Believe it or not, I studied evolutionary biology quite a bit at both the undergraduate and graduate levels, and I’ve read more scientific papers than I can count. So here’s a humble suggestion:

You’ll understand our arguments better (and perhaps be much better able to critique and refute them!) if you use with great caution any working hypotheses you have that ID proponents don’t understand the science they are talking about.

Thanks again for writing—I am not upset by your inaccurate accusations and I do appreciate your civil tone, and I truly hope we can have a friendly lunch sometime.

In sincere friendship,

Casey

Casey,

This will be my last contribution to this thread. Let me begin and end with my most important comment -- the one I came here to make. You and I bring very different perspectives to this conversation. My goal was not to get you to share my perspective, or even to understand it. My goal was to create a little more space in the public discourse for both of us. Specifically, I wanted you to see that one of your initial claims was a falsehood about the evidence explained by common descent, and I also wanted to make it clear that both of us could reasonably see our preferred explanation (descent for me, design for you) as viable in the context of primate genomics. I thought we made some good progress on those counts. You have repeatedly agreed that common descent has explanatory power, and I have reiterated my position that design is neither wrong nor uninteresting. I hope we both keep those things in mind.

Now just some comments in response to your long recent pieces on this thread.

1. Design is unfalsifiable to whatever extent the postulated designer is capable of acting in the world. If the designer (like the Creator God) is omnipotent, then it is impossible to rule out deliberate design in any place at any time. This is a necessary conclusion that can only be avoided by restricting the expected actions/motives of the designer. You claim that "shared non-functional similarities" can falsify "common design," and that's true only if you have defined "common design" in a fairly restricted way. What such similarities don't do -- cannot do -- is rule out the action of a designer. (That designer could have other reasons for doing things the way she does, meaning that "shared non-functional similarities" could evince design just as strongly as any other genomic feature.) That's what I mean when I say that design is unfalsifiable, and I hope that clarifies things.

2. You doubt that I see descent as falsifiable because you equate "being convinced" with "considering to be unfalsifiable." Common descent works as an explanation, and what you have failed to do is demonstrate to me any case in which it has in fact failed. Why might this be?

Well, notably (to me), you have steered the conversation away from primate genomics all the way to the root of the tree of life, avoiding any specific claim regarding the role of design in the structure of primate genomes, which of course is the context of the thread and of all of my comments. I think you have done this because you view the world (and me) in ways that are fantastically different from how I see the world (and you). And so you are less interested in primate genomics than you are in the view of life that you hold, a view that to me seems (let me repeat: seems) to view evolutionary postulates as weird and unlikely and design proposals as obvious and powerful. This drives our conversation, regrettably, away from the careful consideration of primate genetics and genomics and, even more regrettably, away from the interesting but as yet unarticulated ways in which design concepts might be applied there. And so, you are willing to label the work of evolutionary geneticists as "ad hoc epicycles," when in fact common ancestry explains primate genomes and human chromosome 2 extremely well, accounting for all of the observations of interest (not just the telomere-like repeats on chromosome 2, the only aspect you have chosen to address) and while, despite my challenging you to show me how design accounts for these same data, you have written nothing about why and how (for example) human chromosome 2 shows evidence of "design."

And so I interpret your comments about falsifiability to indicate little about the explanatory power of common descent, but much about our differing perspectives.

3. Returning to the concept of explanation I used above, let me note that if you wish to falsify common descent, then you must produce data or observations that cannot be explained by common descent, in principle. (This is the case for any scientific explanation.) Such observations might include strongly anachronistic fossil finds, inexplicable genetic/genomic features, instantaneous appearance of lineages without precursors. For me, the bar will be set at about the same level as it would be for embryonic development of the human cerebral cortex; I currently assume that this structure arises from simpler precursors by typical embryological processes without notable explanatory gaps, even though our knowledge of these processes is famously incomplete. Someone could falsify my theory, for sure, but the data would have to be remarkable to say the least. In other words, both theories are falsifiable, but both are so well established that the falsifying data must take the form of something dramatically more convincing than phylogenetic uncertainty or complexity that is readily accounted for by the theory itself.

4. You sense that I "assume" that you don't understand the papers that you read. That's not quite right. I have concluded that you often (perhaps typically) do not understand evolutionary biology based on what you write and say about it. One example is your uncritical view of recent work from Biologic Institute. Gauger and Axe did some nice biochemistry, but failed to address an evolutionary hypothesis. (Note that I'm not saying that they failed to do a coherent experiment; more fundamentally, they failed to ask a coherent question wrt evolutionary change.) If you had a strong understanding of evolution, you would know that the experiment is not relevant to evolutionary theory. This is a glaring error on your part. Another example is your recent characterization of findings that confirm the influence of epistasis on the speed of evolutionary adaptation. It's bad enough that you think that these findings damage evolutionary explanation; worse, you erroneously claim that these interactions caused "fitness to decrease." Perhaps you just made a mistake, in which you confused "deceleration" with "going backwards," but the whole tone of that piece is wrong. Either you misunderstood the work (and its context) or you misrepresented the findings (probably unintentionally). Neither bolsters your credibility as an analyst of evolutionary biology. Finally, in the current thread you enthuse about Richard Sternberg's comments on telomere-like repeats in human chromosome 2, and you apparently believe that those comments undermine a common descent-based explanation for the apparent fusion event. If you understood that explanation, you would take a different view of Sternberg's comments. At the very least, you would note that the fusion scenario explains multiple features of human chromosome 2 (see Figure 2 in the original 1982 report), not merely those repeats.

Those are just a few quick examples. You're right that I have a low estimation of your grasp of the sweep of evolutionary biology, and only you could change that. I think it would be pretty easy to change, but I can be a little too romantic sometimes.

Now, let me end where I began. First, while I don't think you are a reliable or effective commentator on evolutionary biology, I do think that you could do better. You might, for example, simply do more to acknowledge the strength of common descent and the ability of the scientists you critique. You might, say, make it clear that you really understand the human chromosome 2 fusion hypothesis, that you can see how it works well, but that you want to point to some aspects of the hypothesis that can admit alternative explanations. (This isn't merely being respectful or generous. It's being honest.) And you and your colleagues could do more to show how design works as an explanation. But much more importantly, regardless of my opinion on your abilities as a critic, I affirm the interesting and valid nature of design as a perspective on the world and as an adjunct to common descent. And I affirm the validity of your strong preference for design-based explanation. My preferences are different -- very different, it would seem -- but that just means that we could have a really interesting and stimulating lunch sometime. It doesn't have to mean that we are enemies.

Dear Dr. Matheson,

In your most recent comment, a number of your claims centered on accusations that I “significantly misunderstood” or “misrepresented” various papers. I fear that in making these accusations, in fact it is you have significantly misunderstood or misunderestimated my arguments. In this final comment I will address those misconceptions:

Misunderstanding 1:
Regarding the importance of ‘function’ you write:

“you're wrong to claim that when one finds a function for one pseudogene that one has thereby cast doubt on common descent.”

I reply: I have never argued anything like this, nor has anything I have said contravened anything you said in the entire paragraph of your comment from which this quote is taken.

I think you have significantly misunderstood my argument. In my comments, I've made it very clear that common descent can explain shared functional similarities and I never argued that shared functional similarities (especially when they fit into a nested hierarchy) cannot be explained by common descent. So if a pseudogene turns out to be functional (and its distribution fits a nested hierarchy) then that is perfectly compatible with common descent. However, such evidence of function also refutes an argument against common design.

In case you missed my argument, I will repeat it one more time, as I have written for example:

“Functional morphological and genetic similarities between humans and apes could be the result of common design just as much as common descent.”

“Common Descent:
(a) Does explain shared functional similarities (that fit into a nested hierarchy).”

So I think I've pretty clearly not intimated that shared functional similarities which fit a nested hierarchy refute common ancestry.

Misunderstanding 2:

You also write: “you have significantly misunderstood the 2007 MBE paper; you mistakenly concluded that the authors' conclusions cast doubt on human/chimp common ancestry.”

I reply: I never argued that the authors of that paper themselves disbelieve human/chimp common ancestry. In fact, in my prior comment I took care to explain the explanations (I would call them 'epicycles') the paper uses retain common descent in light of the huge amounts of human genomic data that conflicts with the standard phylogeny of hominids. Thus I wrote in my prior comment:

"Of course the purpose of the article isn’t to challenge common ancestry but to save it from this bad data by asserting in fairly ad hoc fashion that some alleles didn’t become fixed into the population of our ancestors at the same time as most of the rest of the genome."

You then write: “Maybe you should re-read the paper more carefully. You might focus on the third paragraph of the Introduction.”

You obviously have not read my post on this paper. I respectfully suggest that you re-read my original post (linked from Point 4 of my article above) on this very paper where I quoted the precise paragraph you cite (the third paragraph of the introduction) in full and stated:

But of course the purpose of the article isn't to challenge common ancestry but to save it through ad hoc explanations of this bad data. The article explains away the contradictory data in this way:To understand why regions in the human genome can differ in their evolutionary history, it needs to be acknowledged that genetic lineages represented by DNA sequences in the extant species trace back to allelic variants in the shared ancestral species. In here, these variants persist until they join in their most recent common ancestor (MRCA). Some genetic lineages, however, do not coalesce in the progenitor exclusively shared by humans and chimpanzees. They enter, together with the lineage descending from the gorilla, the ancestral population of all 3 species, where any 2 of the 3 lineages can merge first. Thus, in two-thirds of the cases, a genealogy results in which humans and chimpanzees are not each other's closest genetic relatives. The corresponding genealogies are incongruent with the species tree. In concordance with the experimental evidences, this implies that there is no such thing as a unique evolutionary history of the human genome. Rather, it resembles a patchwork of individual regions following their own genealogy. (internal citations omitted)So now, when a gene points in the wrong evolutionary direction, evolutionists just assume (quite conveniently) that the allele in question didn't become fixed into the population of our ancestors at the same time as most of the rest of the genome. Yet another ad hoc epicycle is used to explain away why a whopping "23% of our genome" does not place humans as most closely related to chimpanzees, contradicting the standard evolutionary tree.

Is the statement that "[t]he human genome is a mosaic with respect to its evolutionary history" just a sanitized way of saying 'vast portions of our genome tell contradictory stories about our alleged ancestry with apes'?

So again, the problem here is that massive amounts of human genetic data conflicts with a nice, neat nested hierarchy predicted by common descent. They may find ad hoc explanations for this quirky data. But I as someone who is thinking critically about these issues, I do not find this repeated appeals to ad hoc epicycles to explain away contrary data convincing.

I did not misunderstand the MBE paper and in fact my description of the paper in my prior comment is a good summary of the third paragraph of the introduction.

Misunderstanding 3:

Finally, regarding Fan et al. you write:

And in my view, you have significantly misrepresented the discussion by Fan et al. of the relatively high divergence seen in the telomere repeats within human chromosome 2. They didn't have "bad data" and their arguments are well documented.

I reply: I’m very open to the possibility that I got something wrong Dr. Matheson, but unfortunately your comment has not identified anything that I got wrong in my interpretation of this paper.

Regarding ‘bad data’—normally I have been using that term as a synonym for ‘quirky data’ that doesn’t fit squarely with the predictions of a hypothesis. You have cautioned me not to use the term ‘bad data’, and perhaps that is wise, because perhaps ‘bad data’ would normally imply data that was collected when an experiment went wrong.

But in the case of Fan et al., regardless of which definition of ‘bad data’ we adopt, the paper actually suggests that it found both types of ‘bad data’: they found data that didn’t fit neatly with the fusion hypothesis, and they also cite experimental error as one of the possible explanations for why there is high divergence in the telomere repeats. As Fan et al. write:

If the fusion occurred within the telomeric repeat arrays less than ~6 Mya, why are the arrays at the fusion site so degenerate? The arrays are 14% diverged from canonical telomere repeats (not shown), whereas noncoding sequence has diverged (3) Some array degeneracy could be a consequence of sequencing errors. (emphasis added, internal citations removed)

Regarding (3), they appeal to “sequencing errors.” So there you have it: the ‘bad data’ (e.g. highly divergent telomeric repeats that don’t fit neatly with the fusion hypothesis) is the result of ‘bad data’ (e.g. experimental error). How convenient!

Finally, you write: “What I object to is not your preferences or your unconventional ideas, but the occasional lapse in which the science is ignored or oversimplified.”

I reply: I’m not perfect and I’m more than happy to acknowledge that sometimes I make mistakes. But in these cases you have cited here, I’m also more than happy to let the reader decide whether your consistent accusations that I am ignoring or misrepresenting data are accurate.

If I might humbly make a suggestion:

With all due respect Dr. Matheson, you will never fully appreciate ID arguments if you constantly assume (and accuse) that we simply don’t understand the papers we’re writing about.

Nobody is perfect—myself very much included here—but generally speaking we do understand the papers we’re writing about. Believe it or not, I studied evolutionary biology quite a bit at both the undergraduate and graduate levels, and I’ve read more scientific papers than I can count. So here’s a humble suggestion:

You’ll understand our arguments better (and perhaps be much better able to critique and refute them!) if you use with great caution any working hypotheses you have that ID proponents don’t understand the science they are talking about.

All the best to you as well, and thanks again for joining in the discussion.

Sincerely,

Casey

Dear Dr. Matheson,

Thanks for your kind reply to my comment. You wrote that “the ‘common design’ hypothesis” is “unfalsifiable”. I find the argument unpersuasive for two reasons:

(1) In my previous comment, I pretty clearly explained how one can falsify common design—by finding shared non-functional similarities. Designers generate structures that have function, and when we find shared non-functional similarities, this is not well-explained by common design, but IS well explained by common descent.

(2) Ironically, your latest reply suggests that you do not treat common descent in a falsifiable manner.

Regarding (2), you make various comments which leads me to believe you are not willing to treat common descent in a falsifiable manner. For example, you wrote: “You have provided extensive commentary on your own doubts about common descent, none of which I find convincing or illuminating” and “you have not weakened the case for common descent.” You further state “None of those struggles casts doubt on common ancestry.”

At this point, either one of two things is true: Either the data I have cited in fact doesn’t weaken the case for common descent, or you are not willing to treat common descent in a falsifiable fashion. I think it is the latter, and that you would not allow any type of data to challenge common descent.

If we are to treat this issue fairly, I think the kind of data I discussed is exactly the type of data which should weaken common descent,

Common descent predicts that traits be distributed into a pattern which can be fit into a nested hierarchy. But this is not what we are finding. As the New Scientist article I cited earlier states:

"For a long time the holy grail was to build a tree of life," says Eric Bapteste, an evolutionary biologist at the Pierre and Marie Curie University in Paris, France. A few years ago it looked as though the grail was within reach. But today the project lies in tatters, torn to pieces by an onslaught of negative evidence. Many biologists now argue that the tree concept is obsolete and needs to be discarded. "We have no evidence at all that the tree of life is a reality," says Bapteste. That bombshell has even persuaded some that our fundamental view of biology needs to change.[1]

Now before going further we have to distinguish between the mental states of scientists who are reporting data that challenges the tree of life, and the data itself. I’m sure that Bapteste believes that processes like horizontal gene transfer can explain why some of the data does not fit into a nested hierarchy. (Of course, this very article admitted that the non-tree-like nature of the data applies well beyond the relationships of gene-swapping microorganisms, as it observes "the evolution of animals and plants isn't exactly tree-like either"). By using ad hoc explanations, many of these scientists protect common descent from falsification.

So of course Bapteste (and many other scientists I’ve cited) are committed evolutionists. But this doesn’t mean that the data they are reporting doesn’t challenge common descent.

Regardless of what ad hoc explanations they give for the bad data, the problem remains that the data cannot be fit into nested hierarchy predicted by common descent. As the New Scientist article continued:

The problems began in the early 1990s when it became possible to sequence actual bacterial and archaeal genes rather than just RNA. Everybody expected these DNA sequences to confirm the RNA tree, and sometimes they did but, crucially, sometimes they did not. RNA, for example, might suggest that species A was more closely related to species B than species C, but a tree made from DNA would suggest the reverse.

There’s a lot of data out there where this same problem is encountered (see my previous comment for a few examples). If massive amounts of genetic data that cannot be organized into a nested hierarchy don’t in some way ‘weaken’ the case for common ancestry or ‘cast doubt’ at some level on common ancestry, then what would? Is there anything at all that can challenge common ancestry? I’m not sure if you would say ‘yes’.

(Note: Contrary to your claims, I quite clearly and plainly laid out the kind of data that can falsify common design: shared non-functional similarities. So I have shown how my model is testable and falsifiable under various circumstances)

The New Scientist article continues:

[Michael] Syvanen recently compared 2,000 genes that are common to humans, frogs, sea squirts, sea urchins, fruit flies and nematodes. In theory, he should have been able to use the gene sequences to construct an evolutionary tree showing the relationships between the six animals. He failed. The problem was that different genes told contradictory evolutionary stories. This was especially true of sea-squirt genes. Conventionally, sea squirts--also known as tunicates--are lumped together with frogs, humans and other vertebrates in the phylum Chordata, but the genes were sending mixed signals. Some genes did indeed cluster within the chordates, but others indicated that tunicates should be placed with sea urchins, which aren't chordates. "Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another," Syvanen says.

Thus, even among higher organisms, "[t]he problem was that different genes told contradictory evolutionary stories," leading Syvanen to say, regarding the relationships of these higher groups, "We've just annihilated the tree of life."

Such words to not entail mere “struggles to develop specific phylogenies.” It represents a wholesale struggle to fit the data into a tree of life. As W.F. Doolittle says:

"Molecular phylogenists will have failed to find the 'true tree,' not because their methods are inadequate or because they have chosen the wrong genes, but because the history of life cannot properly be represented as a tree."[2]

Of course Doolittle thinks HGT can solve these problems at the base of the tree of life, but if you’ll notice my prior comment found that these phylogenetic incongruities are appearing all throughout the tree of life, even up to its higher branches. As Carl Woese summarizes the situation like this: “Phylogenetic incongruities can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves.”[3]

If you look at my previous comment, many of the papers I cited were forced to appeal to convergent genetic evolution to explain why genetic similarity was appearing where it was found. Thus…

Many shared functional genetic similarities I cited are appearing in places where they cannot be explained by common descent.

Again, if the extensive data that I cited does not cast common descent into some kind of doubt, then I would argue that your statement is a good example of the fact that many evolutionary biologists treat common descent in an unfalsifiable manner.

So while you might feel your comments confidently assert the strength of common ancestry, I think it shows something very different: I think it shows that you are not treating common descent as a falsifiable hypothesis because you will not admit that large quantities of genetic data that cannot be fit into a nested hierarchy (and cause evolutionary scientists to resort to inferring ‘convergent genetic evolution’) can at least “cast doubt” on or “weaken” the case for common ancestry. If that doesn’t cast at least some doubt or in some way weaken the case for common ancestry, what would?

You minimized this data by calling it “several pointers to phylogenetic uncertainty.” Again, I have no doubt that Michael Syvanen is an evolutionary scientist but his words don’t intimate a bit of mere uncertainty: “We've just annihilated the tree of life.”

And looking at the papers I cited in my prior comment, some of the phylogenies where we see ‘uncertainties’ are pretty significant – like the basic relationships of major animal groups.

But let’s call them mere ‘uncertainties’. This is how paradigms fall—more and more ‘uncertainties’ develop, and defenders of the paradigm are forced to resort to more and more epicycles to explain the quirky data (OK, I won’t say “bad data” this time :) ) Eventually the paradigm collapses—and from the kind of language I’m seeing scientists use above, I think that we’re seeing more than just a few quirks in the data. The genetic data simply cannot be fit into the nested hierarchy predicted by common descent.

And there’s a lot of quirky data out there where common ancestry has failed to explain the shared similarities we observe among living organisms. We’ve discussed this data a lot her on ENV, and for those who are interested in such links, please see

Summary of Breakdowns in Attempts to Reconstruct the Tree of Life

A Primer on the Tree of Life

Venter vs. Dawkins on the Tree of Life -- and Another Dawkins Whopper

For Darwin Day: False Facts & Dawkins' Whopper

More Points on ERVs

Revisiting an Old Chestnut: Retroviruses and Common Descent (Updated)

Convergent Genetic Evolution in Lichen Species

Inconvenient Fungus Genetic Data Leads to Epicycles in the Tree of Life

Science Article Acknowledges Convergent Similarity Is "Contrary to Expectations" of Neo-Darwinism

Common Design in Bat and Whale Echolocation Genes?

Implications of Genetic Convergent Evolution for Common Descent

Convergent Genetic Evolution: "Surprising" Under Unguided Evolution, Expected Under Intelligent Design

These articles don't just discuss 'struggles' to explain a few limited phylogenies. They discuss a failure to construct many parts of the tree of life, from top to bottom.

In closing you wrote: “I think we can disagree respectfully”. I appreciate you saying that and hope that this is the start of increased civil dialogue.

Sincerely,

Casey

References Cited:

[1.] Graham Lawton, “Why Darwin was wrong about the tree of life,” New Scientist (January 21, 2009) (emphases added).

[2.] W.F. Ford Doolittle, "Phylogenetic Classification and the Universal Tree," Science, Vol. 284:2124-2128 (June 25, 1999).

[3.] Carl Woese "The Universal Ancestor," Proceedings of the National Academy of Sciences USA, Vol. 95:6854-9859 (June, 1998).

The high similarity of human and ape DNA applies only when sequences of major differences are ignored. The 98% similarity applies only when looking at differences of one or two insertions, deletions or changes in a row, probably due to very recent mutations of both species. If significant differences are also considered, the similarity is in the low 90%.

Hi Casey, thanks for the response. You addressed my concern about the "not at all" comment very well, and I think your meaning is a lot clearer now.

As you know, I consider the "common design" hypothesis to be unfalsifiable as well as fully compatible with common descent (given the likelihood that the "designer" is omnipotent or at least super-potent). And as you know, I consider the explanatory power of common descent to be immense. You have provided extensive commentary on your own doubts about common descent, none of which I find convincing or illuminating. (Personal preferences here, I'm sure.)

For example, you emphasize issues of "function" when it comes to the genomic features that I believe that ID should attempt to explain, but in fact "function" (or lack thereof) is of little relevance in explaining the positions or behavior of mobile genetic elements or the postulated chromosome fusion event in the human lineage or of synteny in general. A biologist does not –- and need not -- assert that a particular pseudogene or retroelement or repeat is functionless when invoking common descent to explain the element's placement in a genome. In fact, when it comes to (say) synteny -- the arrangement of genes of known function in specific order on a chromosome -- common descent proposes an explanation for the pattern while explicitly affirming the function of the elements in question. You're right that commonalities in the placement of "non-functional" elements are strong indicators of common ancestry, but you're wrong to claim that when one finds a function for one pseudogene that one has thereby cast doubt on common descent.

You also cite various struggles to develop specific phylogenies. None of those struggles casts doubt on common ancestry, any more than doubts about the parentage of a person casts doubt on their humanity. You may feel that these citations should lead to a bit less hubris on the part of scientists when discussing a particular phylogenetic tree, and I would agree with that. But you haven't provided an argument against common descent with your several pointers to phylogenetic uncertainty.

My intention is not to disparage your preference for a design hypothesis, nor is it to claim that design has nothing to do with structural commonalities in primate genomes. I only seek to make it clear that you have not weakened the case for common descent.

You refer to "bad data," and I think you should avoid such talk. (My opinion.) Especially when you discuss the structure of chromosome 2, you give the impression that scientists are facing data that contradict a favored hypothesis but are choosing to concoct bogus explanations to protect the hypothesis. I read the paper you referenced in both such cases in this thread, and discovered that you are quite mistaken about "bad data." In fact, you have significantly misunderstood the 2007 MBE paper; you mistakenly concluded that the authors' conclusions cast doubt on human/chimp common ancestry. Maybe you should re-read the paper more carefully. You might focus on the third paragraph of the Introduction. And in my view, you have significantly misrepresented the discussion by Fan et al. of the relatively high divergence seen in the telomere repeats within human chromosome 2. They didn't have "bad data" and their arguments are well documented.

Anyway, I think we can disagree respectfully. I don't see genomes the way you do, nor do I find design arguments convincing. What I object to is not your preferences or your unconventional ideas, but the occasional lapse in which the science is ignored or oversimplified. And I have yet to see a serious attempt to explain genomic structures using design. It's understandable, since such an effort would require enormous effort and talent. But it hasn't happened, and I think ID folks should be a bit more forthright about that.

Best regards,
Steve Matheson

Dear Dr. Matheson,

Thank you for joining in the discussion here. I’ve been traveling today so this reply is coming from 40,000 feet.

Let me say first off that I think that my use here of the word “bolster” without qualification left some unintended ambiguity about what I was trying to say. Shared functional genetic similarities can often be explained by common descent (that is, when they fit into a nested hierarchy – more on this below), so in that sense it does “bolster” the case for common ancestry. But such shared functional genetic similarities do not ‘bolster’ the case for common ancestry over common design, because I believe that common design can explain shared genetic similarities equally well. I think that if I were to rewrite that sentence to be more precise, I would say it like this:

Does this shared functional genetic similarity demonstrate neo-Darwinian evolution and human/ape common ancestry over common design? Not at all.

You then wrote:

“In fact, genetic and genomic analysis is very strong evidence for human/chimp common ancestry. Or, more accurately in my view, common ancestry provides excellent explanation for genomic similarity between humans and chimps. To assert otherwise is to assert a falsehood, one that no knowledgeable reader would identify as reasonable.”

In reply, I respectfully disagree here with Dr. Matheson. Since designers regularly re-use parts that work in different designs, mere functional genetic similarity can be explained by common design just as much as it can be explained by common descent. Paul Nelson and Jonathan Wells elaborate on this point:

"An intelligent cause may reuse or redeploy the same module in different systems, without there necessarily being any material or physical connection between those systems. Even more simply, intelligent causes can generate identical patterns independently."

(Paul Nelson and Jonathan Wells, "Homology in Biology," in Darwinism, Design, and Public Education, (Michigan State University Press, 2003).)

Even the neo-Darwinian evolutionist (and ID critic) Francis Collins concedes that as long as we are talking about shared functional similarity, common design is a viable explanation, as he writes in The Language of God regarding shared functional genetic similarity:

This evidence alone does not, of course, prove a common ancestor; from a creationist perspective such similarities could simply demonstrate that God used successful design principles over and over again.

(Francis Collins, The Language of God, p. 134 (Free Press, 2006).)

Thus, regarding Dr. Matheson’s examples of shared synteny or the chromosome 2 situation (e.g. human chromosome 2 resembles other chromosomes in apes), at most all these examples do is show shared functional genetic similarities between humans and apes. Since shared functional genetic similarities can be explained by common design equally as well as by common descent, such data does not help us to discriminate between intelligent design and neo-Darwinian evolution.

So can we discriminate between common design and common descent? I think that there is some data that can help us.

In The Language of Science and Faith Giberson and Collins again imply that functional genetic similarity can be explained by common design, because they argue against common design by observing that non-functional DNA (what they call “’broken’ DNA”) is best explained by common ancestry:

Although some still argue that DNA similarities do not prove common ancestry—God might have reused the same DNA Patterns for similar animals—the details have ruled out that conclusion.

(Giberson and Collins, The Language of Science and Faith, p. 43 (InterVarsity Press, 2011).)

Why do they argue that some genetic similarities point to common ancestry—well, in the next paragraph they cite what they call “broken DNA”—i.e. nonfunctional DNA—which is best explained by common descent. Why is that? Well, designers tend to produce structures that are functional, whereas unguided mutation and evolutionary processes are very good at degrading or destroying function. So when we find non-functional structures, that is better explained by unguided mutation, and thus shared non-functional structures are better explained by common descent than common design.

None of this contradicts anything I’ve been arguing here. In fact, I am in complete agreement with Collins and Giberson on this point. As I explained to commenter Jeremy: “A key word there is ‘functional,’ because I agree that nonfunctional similarities are better explained by unguided evolutionary processes. This shows the predictive power of intelligent design: ID predicts that structures will have function, so when we find non-functional structures (whether shared or not) those are not best explained by ID.”

But as I further explained to Jeremy: “The problem for those who make the ‘nonfunctional genetic similarities’ argument, is that many examples of supposed shared ‘non-functional’ similarities are turning out to be functional.”

Thus, Dr. Matheson, when you cite allegedly nonfunctional DNA like pseudogenes or mobile genetic elements, these could potentially point to common ancestry if they indeed turn out to be nonfunctional. But the data is increasingly not pointing in that direction. I’m open to the possibility but the data seems to be continually foreclosing that option due to the tremendous amount of function being discovered for noncoding DNA (Jonathan Wells' endnotes in The Myth of Junk DNA provide references that just begin to document this evidence).

If shared non-functional similarity can point to common descent, is there a class of data that can unambiguously point to common design? Yes.

When we find shared functional biological similarities that do not fit well within a nested hierarchy, requiring what evolutionary biology calls convergent evolution or homoplasy, I would argue this data is best explained by common design. Homoplasy / convergent evolution represent shared functional similarity that does not result from common ancestry. In many cases, we’re talking about complex structures that are claimed to result from convergence. ID proponents find this data very interesting because this is exactly what you would expect if an intelligent agent was re-using complex functional components in different designs.

And in fact, we see this kind of data all over the place. There are numerous instances where genetic data does not fit into the nice, neat nested hierarchy predicted by common descent, and the data instead shows that similarity is popping up in places unpredicted by common ancestry. As a New Scientist paper explained in 2009, “The problem was that different genes told contradictory evolutionary stories,” and “research suggests that the evolution of animals and plants isn’t exactly tree-like either.” This problem led one evolutionary scientist to say regarding the relationships of these higher groups, “We’ve just annihilated the tree of life.”[1] Let’s look at a few examples where scientists have struggled to create a tree of life because the data could not fit into a nice neat nested hierarchy predicted by common descent:

A 2009 paper in Trends in Ecology and Evolution notes that: “A major challenge for incorporating such large amounts of data into inference of species trees is that conflicting genealogical histories often exist in different genes throughout the genome.”[2] Similarly, a paper in the journal Genome Research studied the DNA sequences in various animal groups and found that “different proteins generate different phylogenetic tree[s].”[3]

A study published in Science in 2005 tried to construct a phylogeny of animal relationships but concluded that “[d]espite the amount of data and breadth of taxa analyzed, relationships among most [animal] phyla remained unresolved.”[4] Again, the problem lies in the fact that trees based upon one gene or protein often conflict with trees based upon other genes. Their study tried to avoid this problem by using a many-gene technique, yet still found that “[a] 50-gene data matrix does not resolve relationships among most metazoan phyla.”

Striking admissions of troubles in reconstructing the “tree of life” also came from a 2006 paper in the journal PLoS Biology, entitled “Bushes in the Tree of Life.” The authors acknowledge that “a large fraction of single genes produce phylogenies of poor quality,” observing that one study “omitted 35% of single genes from their data matrix, because those genes produced phylogenies at odds with conventional wisdom.” The paper suggests that “certain critical parts of the [tree of life] may be difficult to resolve, regardless of the quantity of conventional data available.” The paper even contends that “[t]he recurring discovery of persistently unresolved clades (bushes) should force a re-evaluation of several widely held assumptions of molecular systematics.”[5]

Another study published in Science found that the molecular data implied that six-legged arthropods, or hexapods (i.e. insects) are not monophyletic, a conclusion that differed strikingly from virtually all previous wisdom. The article concluded “Although this tree shows many interesting outcomes, it also contains some evidently untenable relationships, which nevertheless have strong statistical support.”[6]

A paper in the Journal of Molecular Evolution found that molecule-based phylogenies conflicted sharply with previously established phylogenies of major mammal groups, concluding that this anomalous tree “is not due to a stochastic error, but is due to convergent or parallel evolution.”[7] Likewise, a study published in Proceedings of the National Academy of Sciences USA explains that when evolutionary biologists tried to construct a phylogenetic tree for the major groups of birds using mitochondrial DNA (mtDNA), their results conflicted sharply with traditional notions of bird relationships. Strikingly, they even find “convergent” similarity between some bird mtDNA and the mtDNA of distant species such as snakes and lizards. The article suggests bird mtDNA underwent “multiple independent originations,” with their study making a “finding of multiple independent origins for a particular mtDNA gene order among diverse birds.”[8]

So clearly, not all shared functional similarities fit well into the nested hierarchy predicted (and required) by common descent. In these cases, shared functional similarities were NOT very well explained by common descent because they did not fit into a nested hierarchy.

In fact we find shared functional similarities among higher primates that do not fit well into a nested hierarchy. Some of the data I have described in this very article (see point 4 of my article above) here presents genetic data that did not fit well with a nested hierarchy. Let’s focus in on just one particular paper:

A 2007 paper in the journal Molecular Biology and Evolution states:”For about 23% of our genome, we share no immediate genetic ancestry with our closest living relative, the chimpanzee. This encompasses genes and exons to the same extent as intergenic regions. We conclude that about 1/3 of our genes started to evolve as human-specific lineages before the differentiation of human, chimps, and gorillas took place.”[9]The article goes on to state that "[t]he human genome is a mosaic with respect to its evolutionary history." In other words, some parts of the genome tell one evolutionary story while others tell a different, contradictory story. Our genome is not painting a consistent picture of common descent that fits a nice, neat nested hierarchy predicted by common descent. The paper continues:However, with both amount of data and number of studies increasing, the crux of the matter emerges. Regardless of the type of phylogenetically informative data chosen for analysis, the evolutionary history of humans is reconstructed differently with different sets of data. (internal citations omitted)Of course the purpose of the article isn’t to challenge common ancestry but to save it from this bad data by asserting in fairly ad hoc fashion that some alleles didn’t become fixed into the population of our ancestors at the same time as most of the rest of the genome. Thus, they argue that "[t]he human genome is a mosaic with respect to its evolutionary history”—but this is just a sanitized way of saying ‘vast portions of our genome tell contradictory stories about our alleged ancestry with apes’.

And in fact when compared with molecular data, morphological data often paints a contradictory picture of common ancestry as well that does not fit into a nice, neat nested hierarchy. A 2000 article in Nature explains that “Evolutionary trees constructed by studying biological molecules often don’t resemble those drawn up from morphology,” and further explains that this problem extends into attempts to reconstruct human/ape phylogenetic relationships:
So the researchers constructed an evolutionary tree based on 129 skull and tooth measurements for living hominoids, including gorillas, chimpanzees, orangutans and humans, and did the same with 62 measurements recorded on Old World monkeys, including baboons, mangabeys and macaques. They also drew upon published molecular phylogenies. At the outset, Wood and Collard assumed the molecular evidence was correct. “There were so many different lines of genetic evidence pointing in one direction,” Collard explains. But no matter how the computer analysis was run, the molecular and morphological trees could not be made to match15 (see figure, below). Collard says this casts grave doubt on the reliability of using morphological evidence to determine the fine details of evolutionary trees for higher primates. “It is saying it is positively misleading,” he says. The abstract of the pair’s paper stated provocatively that “existing phylogenetic hypotheses about human evolution are unlikely to be reliable”.[10]
So I think that both shared genetic and morphological similarities between humans and apes do not always not paint a nice, neat and clean picture of alleged human / ape relationships as you claim it does. Far from it. This diagram from Nature explains the disparate phylogenies that are produced:

click here for diagram. (Diagram reprinted by permission from Macmillan Publishers Ltd: Nature, Trisha Gura, “Bones, Molecules or Both?,” Nature, Vol. 406:230-233 (July 20, 2000), copyright 2000.)

So looking at the diagram, it's clear that the morphological and molecular data does not always fit with a nice, neat nested hierarchy.

In summary, I think that some classes of data are best explained by common descent, while some are best explained by common design. Still other data is explained by both common descent and common design. I would argue that the explanatory value of these models cashes out something like this:

Common Descent:
(a) Does explain shared functional similarities (that fit into a nested hierarchy).
(b) Does explain shared non-functional similarities
(c) Does NOT explain shared functional similarities that don't fit into a nested hierarchy (e.g. convergence / homoplasy)

Common Design:
(a) Does explain shared functional similarities (that fit into a nested hierarchy).
(b) Does NOT explain shared non-functional similarities
(c) Does explain shared functional similarities that don't fit into a nested hierarchy (e.g. convergence / homoplasy).

We know that (a) and (c) exist. But the data is increasingly pointing against (b) being prevalent.

Finally, my claim that common design can explain much of this data is not a “blatant assertion,” as you call it. It’s based upon observations of how designers design things. We observe that designers (1) generate complex structures, (2) that are functional, and (3) that they re-use such functional components in different designs. Additionally, intelligent agents are also not obligated and constrained to necessarily distribute those structures into their designs in a manner that has to always fit a nested hierarchy.

And guess what we find in nature? We find: Complex functional parts which are re-used in widely diverse organisms in a manner that often does not fit a nested hierarchy.

I have not made mere assertions, but have explained why common design explains this data by evaluating how designers work when they design things.

In closing, please let me say that I appreciate you writing in and I can assure you Dr. Matheson that as long as you are on this forum, you will be treated with respect and civility, even (and especially!) when people disagree with you. I hope that this comment clarifies things a little.

Sincerely,

Casey

References Cited:

[1.] Graham Lawton, “Why Darwin was wrong about the tree of life,” New Scientist (January 21, 2009) (emphases added).

[2.] James H. Degnan and Noah A. Rosenberg, “Gene tree discordance, phylogenetic inference and the multispecies coalescent,” Trends in Ecology and Evolution, Vol. 24(6) (March, 2009).

[3.] Mushegian et al., “Large-Scale Taxonomic Profiling of Eukaryotic Model Organisms: A Comparison of Orthologous Proteins Encoded by the Human, Fly, Nematode, and Yeast Genomes,” Genome Research, Vol. 8:590-598 (1998).

[4.] Antonis Rokas, Dirk Krueger, and Sean B. Carroll, “Animal Evolution and the Molecular Signature of Radiations Compressed in Time,” Science, Vol. 310:1933-1938 (Dec. 23, 2005).

[5.] Antonis Rokas and Sean B. Carroll, “Bushes in the Tree of Life,” PLoS Biology, Vol. 4(11): 1899-1904 (Nov., 2006) (internal citations and figures omitted).

[6.] Nardi et al., “Hexapod Origins: Monophyletic or Paraphyletic?,” Science, Vol. 299:1887-1889 (March 21, 2003).

[7.] Cao et al., “Conflict Among Individual Mitochondrial Proteins in Resolving the Phylogeny of Eutherian Orders,” Journal of Molecular Evolution, Vol. 47:307-322 (1998).

[8.] Mindell et al., “Multiple independent origins of mitochondrial gene order in birds,” Proceedings of the National Academy of Sciences USA, Vol. 95: 10693-10697 (Sept. 1998).

[9.] Ingo Ebersberger, Petra Galgoczy, Stefan Taudien, Simone Taenzer, Matthias Platzer, and Arndt von Haeseler, "Mapping Human Genetic Ancestry," Molecular Biology and Evolution, Vol. 24(10):2266–2276 (2007).

[10.] Trisha Gura, “Bones, Molecules or Both?,” Nature, Vol. 406:230-233 (July 20, 2000) (emphasis added).

Phil, your comments reveal profound ignorance of the topic of chromosome fusion (and, in general, on chromosomal rearrangements) and on the specific issue of the origins of chromosome 2. That is why you can't "imagine" how it would go. Here is a basic outline (of the postulated scenario).

The common ancestor of humans and chimps had two chromosomes, call them A and B, among its collection. After the lineage leading to chimps and the lineage leading to humans diverged, a fusion of those two chromosomes (call it AB) occurred in an animal in the human lineage. That new chromosome was either favored by selection or it became prevalent in the population for another reason. However it came to pass, all of the organisms in that lineage eventually came to have AB instead of A + B. That lineage gave rise to humans.

Note that such a scenario would apply to any genomic feature that differs between two closely-related species/lineages. There's nothing remarkable about the explanation.

Two further notes on your comment.

1. Chromosomal rearrangements are common in animal genomes. They can take various forms. The fusion of two chromosomes, as is thought to have occurred since the divergence of humans and chimps, is not extraordinary and requires no extraordinary explanation. That it was maintained in the human lineage is indeed interesting, but not profoundly inexplicable as you assert.

2. The rearrangement in question would have occurred in one organism. Not between two species. I'm not sure why you thought otherwise.

It is understandable that, as a historian and a soldier, you would not be well-informed about genomic biology. What is less easy to grasp is why you would mock science that you clearly haven't tried to understand.

Folks, the original article boils down to two important claims. One is a falsehood and the other is an interesting and debatable assertion.

The falsehood: "Does this functional genetic similarity bolster neo-Darwinian evolution and human/ape common ancestry? Not at all."

In fact, genetic and genomic analysis is very strong evidence for human/chimp common ancestry. Or, more accurately in my view, common ancestry provides excellent explanation for genomic similarity between humans and chimps. To assert otherwise is to assert a falsehood, one that no knowledgeable reader would identify as reasonable.

If the author meant to say that such evidence does not by itself establish common ancestry, or that such analysis does not rule out "design," then we can have an interesting discussion. But the statement seems to claim that genetic evidence does not "bolster" common ancestry, "at all," and that's nonsense. (It could be that the author really didn't intend to go that far in disparaging common descent.)

More interesting is this claim: "functional biological similarity is explained by common design just as well as it's explained by common descent."

To make that claim into something more than a blatant assertion, the author would need to point to analysis of primate genetics and genomics that support the claim that primate "morphology" explains common genetic and genomic elements, i.e., that primate genomes must be the way they are in order to undergird primate "morphology" or function or whatever. Whether it's synteny, or the chromosome 2 situation, or unitary pseudogenes, or mobile genetic elements, the burden is on the design theorist to explain how "common design" accounts for these features. To assert that common descent does not account for them is neither remotely accurate nor necessary in the course of arguing for common design.

My point is not that the assertion of "common design" is wrong, or that the author is wrong to prefer such an explanation, only that he has no evident justification for claiming that his explanation is just as good as common descent. To bolster his case, he would need real analysis, not blatant assertion.

I was going to post this with the ancestry article recently at your blog, but the article disappeared…
Yet I think you will like this--

It seems the common ancestor explanation of shared introns should be questioned due to this finding:

http://www.sciencedaily.com/releases/2009/12/091210111148.htm
"Remarkably, we have found many cases of parallel intron gains at essentially the same sites in independent genotypes," Lynch said. "This strongly argues against the common assumption that when two species share introns at the same site, it is always due to inheritance from a common ancestor."

For years the 'only explanation' for the intron in a shared site was common ancestor. But that explanation was not due to observation, but rather induction. Here we have an actual observation that shows the induction faulty.
I haven't seen this finding discussed as much as I thought I would. Am I misunderstanding?

A fusion? I will be absolutely honest here, as a doctorate in History and a soldier I am at a loss to imagine what naturalistic force would result in a fusion between the genes two utterly different animals? Is this 'event' supposed to have occurred BEFORE the lines split, or is it supposed to be the reasons the lines split, or is that just something else we are supposed to take as a matter of materialistic faith?
Fascinating piece, Casey - what I could take away from it. Perhaps some more homework is in order.

Mr Luskin, that's an impressive commentary.
Thank you for posting it along with the links.

"It is difficult to get a man to understand something when his salary depends upon his not understanding it." Upton Sinclair was quoted in An Inconvenient Truth. I think we can be forgiven in modifying it a little into: “It is difficult to get a man to understand something when his world view depends upon his not understanding it."

For some, the notion that life has a meaning and purpose inevitably leads to the thought of accountability to the giver of meaning and purpose. That’s a very Inconvenient notion, if not truth.

Thank you Casey for all the hard work!

I have not found this information on your website but thought it was interesting.

http://www.ncbi.nlm.nih.gov/pubmed/15716009

Eighty percent of proteins are different between humans and chimpanzees

Abstract

The chimpanzee is our closest living relative. The morphological differences between the two species are so large that there is no problem in distinguishing between them. However, the nucleotide difference between the two species is surprisingly small. The early genome comparison by DNA hybridization techniques suggested a nucleotide difference of 1-2%. Recently, direct nucleotide sequencing confirmed this estimate. These findings generated the common belief that the human is extremely close to the chimpanzee at the genetic level. However, if one looks at proteins, which are mainly responsible for phenotypic differences, the picture is quite different, and about 80% of proteins are different between the two species. Still, the number of proteins responsible for the phenotypic differences may be smaller since not all genes are directly responsible for phenotypic characters.

Thanks for the responses.

Dear J. Preston,

Thanks for the comment in reply. I thought I had already answered your questions but this is helpful to lay the questions and answers out clearly.

Question 1: "What explanatory power does ID offer regarding human chromosome 2?"

I reply: About the same minimal explanatory power that common descent offer for the data we observe in human chromosome 2. Sometimes the data is just what it is and no model predicts it clearly. I would say ID predicts this data no worse than common ancestry.

Also, assuming the evidence for fusion is compelling (a claim that is weakened given the evidence I've raised in this thread), at most all it shows is that humans are descended from ancestors with 48 chromosomes. Those ancestors might have been just as human as you and me. Or they might have been very ape-like. Chromosomal fusion simply does not answer that question.

Question 2: "What potential discovery regarding the status of the fusion event could falsify ID?"

I reply: Assuming for the sake of argument that the fusion evidence could establish human/ape common ancestry (which it cannot), my article above notes that "human/ape common ancestry is compatible with ID." So there are good ways to test ID (for a discussion, please see A Positive, Testable Case for Intelligent Design), but debating human/ape common ancestry is not one of them.

Question 3: "If ID is confirmed regardless of the status of the fusion is it really that strong of an explanation in this case?"

I reply: I'm not sure if I completely understand what you are getting at here. But I’ll take a stab: The case for ID depends on evidence that is far removed from the fusion evidence, so even if human chromosome 2 is the result of a fusion event and somehow this provides evidence that humans and apes share a common ancestor, that would not refute ID. So

I'm not claiming that any model here is a "strong" explanation for what we observe in human chromosome 2, whether we're talking about ID or common descent. So I reject a premise in this question.

Thanks and I hope this helps.

Sincerely,

Casey

Ok, I can see this is going nowhere, but I'd like to give you one more chance to respond to my initial point (which you've ignored twice now). I'll try to be more specific this time...

*What explanatory power does ID offer regarding human chromosome 2?
*What potential discovery regarding the status of the fusion event could falsify ID?
*If ID is confirmed regardless of the status of the fusion is it really that strong of an explanation in this case?

Thanks.

Dear J Preston,

I appreciate your reply but cannot help but point something out: In my experience debating this issue, there are 3 good signs that your opponent is probably out of arguments:

(1) he stops talking about the evidence and starts appealing to authority.
(2) he starts to dispute one's right to disagree with those deemed the "experts"
(3) he starts making declarations that you really agree with him.

Not only did you not address the evidence I raised, but your reply to me did each of those 3 things.

Regarding (1) and (2), you suggested that I should simply accede to the “expert opinion” of the Genome Research paper. Because I didn’t do this, you accused me of “dismissal” of the paper.

Had I "dismissed" the paper, then I would not have addressed its arguments, and you're right that that would not be credible. But that’s not what I did.

Rather than dismissing the Genome Research paper, I read the paper, looked at its results, discussed those results, and argued that evidence it reported didn't fit well with the fusion hypothesis, and I also argued that the authors used weak explanations to explain away the bad data. That isn’t a “dismissal,” and calling it that doesn’t respond to my argument.

Also, rather than explaining why my argument was wrong, you simply requoted from the abstract of the Genome Research paper where it asserts "Human chromosome 2 was formed by the head-to-head fusion of two ancestral chromosomes that remained separate in other primates."

That’s just a headliner statement. What matters is the meat of the paper and what evidence was reported. We already know the paper favors fusion (after all, the point of my entire previous comment was to analyze how they found data that didn’t fit well with the fusion model, and had weak explanations for that data), so that quote doesn't really add to our discussion. The quote from the abstract doesn't fix the quirky data that was reported in the paper, nor does it correct the weaknesses in the paper’s arguments.

Regarding (3), you wrote at the end that “I'm inclined to think you agree with me here.” Well, I it’s difficult for me to agree with your position when you have not responded to my arguments, including those which showed that common ancestry doesn't obviously predict or explain the data we have actually found: It's not just that the data doesn't fit "perfectly" with the fusion hypothesis, but that it appears to only fit with the fusion hypothesis on a weak or trivial level. That's a problem. And even if the fusion evidence was perfect (or even just good), you haven't responded to my argument that this would not demonstrate human/ape common ancestry.

As the title of my article suggests, I'm trying to follow the evidence. If the evidence leads to agreement with those you deem the "experts," that’s fine. If not, that should be fine too. What matters is the evidence. Appeals to authority do not respond to evidence-based arguments.

Ironically, while you label my argument a “dismissal,” it seems you have dismissed my argument without addressing them.

Finally, regarding ID dialoguing with evolutionary scientists, at any given day I probably have at least 1 or 2 dialogues going on with various evolutionary scientists and scholars. So I appreciate the value of this and agree that much good can come from it.

Thanks again for writing in.

Sincerely,

Casey

Mr. Luskin, thanks for responding.

You're right: "perfect" was a bad choice of words on my part. But let's not miss the main point here - no one outside of the ID community denies that human chromosome 2 resulted from a fusion or that it has a striking correspondence with two chimp chromosomes. Just see the first sentence from the abstract of the paper you linked:

"Human chromosome 2 was formed by the head-to-head fusion of two ancestral chromosomes that remained separate in other primates."

No offense, but I don't find your dismissal of the expert opinion from this paper very credible. I would like to humbly offer a suggestion, however. Why not contact the authors of that article directly and politely express your criticisms regarding the "ad hocness" of their conclusions? I think this could result in some really beneficial dialogue. Whether deservedly or not, the ID community has a reputation for not engaging scientists on their on territory, and such a gesture might really go a long way.

But anyway, you said you were willing to accept (at least for the sake of argument) that there is evidence of a fusion. In that case, my previous point still stands: in the instance of human chromosome 2, ID offers no explanatory power whatsoever, while common ancestry offers a ton. Given the direction of your response, I'm inclined to think you agree with me here.

Unless I misunderstand the point you are making, I have never thought of intelligent design as providing a demarcation argument for common ancestry versus not common ancestry.

I have always understood the claim that intelligent design is compatible with both as merely a clarification of what intelligent design asserts.

It is probably needed to counter a belief that some may have that proving common ancestry falsifies intelligent design.

Years ago (1994) I read a book written and self-published by Dr. Periannan Senapathy entitled The Independent Birth of Organisms. (I even have his signature on the endorsement line on the back of the check I sent him.)

His theory does not depend on common ancestry. On the book jacket he says this:

Evolution's critical premise actually rests on another more fundamental premise: that the random chemical reactions and recombinations within the primordial pond could not possibly have produced a genome, even for the most primitive single-celled organism, except by some fantastic accident. But what if the premise is false? What if the primordial pond actually produced an assortment of genes?

He was accused of being a creationist, but as I recall he was merely trying to explain the evidence (sudden appearance of organisms) as he found it.

So, at least at one point in the history of evolutionary thought, there was someone trying to come up with a naturalistic explanation of the fossil record as he perceived it.

Dear J Preston,

Thanks for the comment. You claim that human chromosome 2 "perfectly corresponds to two chromosomes from the chimp genome" and that "just as predicted" by common ancestry "a fusion point was discovered." But in fact the fusion evidence isn't nearly as "perfect" as you claim it is. Moreover, the ad hoc explanations evolutionists use when struggling to explain away the imperfections in the fusion-evidence shows that it’s not at all clear what common ancestry truly “predicts” with regards to chromosomal fusion.

As Richard Sternberg eloquently points out, there are interstitial telomeric sequences found commonly throughout mammalian genomes, but it's just the telomeric sequences in human chromosome 2 that are cherry-picked and cited as evidence for an ancient fusion event:

[O]f all the known ITSs [interstitial telomeric sequences], 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, Ponsá 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.

So the alleged telomeric evidence for fusion isn't really very remarkable.

But you make a very strong claim--that the data "perfectly corresponds to two chromosomes from the chimp genome." But that's hardly the case. Telomeric DNA normally consists of thousands of repeats of a 6-base-pair sequence TTAGGG. Daniel Fairbanks admits in his ardently-pro-common-descent book Relics of Eden that the alleged fusion point in human chromosome 2 only shows 158 repeats, and only "44 are perfect copies of TTAGGG or CCTAA." (p. 27) So if two chromosomes were fused "end-to-end", then a huge amount of alleged telomeric DNA is missing and/or garbled.

In fact one paper in Genome Research found that the alleged telomeric sequences have "degenerated significantly" and "highly diverged from the prototypic telomeric repeats.” The paper is surprised to find this because the alleged fusion event supposedly happened very recently—-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, why are the arrays at the fusion site so degenerate?"

So there are at least two reasons why the evidence for end-to-end fusion isn't so "perfect" as you claim it is: (a) the alleged fusion point in chromosome 2 contains much less telomeric DNA than it should, and (b) the telomeric sequences are highly "degenerate" and thus not what you would expect to find in such a recent fusion event.

The authors of the Genome Research paper then offer various ad hoc explanations for why the alleged fusion-sequence in human chromosome 2 in many respects doesn't actually resemble two end-to-end fused chromosomes. They give three possible explanations for this bad data: (1) they suggest the chromosomes weren't really joined at their ends; (2) they arbitrarily invoke a "high rate of change" in that stretch of DNA, or (3) they suggest there were errors in the sequencing process.

Perhaps any or all of these are possible. The fact that they would resort to the first explanation shows just how not "perfect" the evidence is for end-to-end chromosomal fusion. The fact that they would invoke explanations 2 and 3 shows just how much the observed telomeric DNA diverges from what they expected to find if there was a fusion event. Indeed, when you cite errors in your own experimental methods to explain data that contradicts your hypothesis, that appears quite arbitrary and doesn’t inspire confidence in the hypothesis.

But—-and this is key—-their use of ad hoc explanations to explain away bad data that doesn't fit with the fusion hypothesis leads me to a much larger final point:

You also claim that human chromosomal fusion evidence is "just as predicted" by common ancestry. But what does common ancestry really predict here?

If we didn't find evidence of fusion in chromosome 2, evolutionists might just argue that, contrary to the constraints of parsimony, the primitive trait among hominids is 46 chromosomes, and there was independent chromosomal duplication in various ape lineages which led apes to have 48 chromosomes. Or, evolutionists might claim that fused telomeric DNA was deleted, thereby obliterating genetic evidence of fusion. In fact, that's exactly the sort of approach taken by the Genome Research paper to explain why so much telomeric DNA in fact appears to have been deleted or garbled!

So the evidence for fusion isn't so "perfect" and we see that when faced with that data, evolutionists resort to ad hoc explanations to explain away the bad data. So what does common ancestry really “predict” here? Based upon the behavior of evolutionists, I'm not sure. But I am pretty sure of this: if there was zero evidence for human chromosomal fusion, proponents of common ancestry would not question their model but would find ways to explain away the bad data, just like the Genome Research authors did. Again, what does common ancestry really “predict” in practice here? Not much of a "prediction” in my opinion.

You wrote: “falsifiable data is where it's at.”

I reply: That’s fine with me. If common ancestry really makes a hard-and-fast falsifiable prediction here, will you admit that the significant differences between true telomeric sequences and what we find in human chromosome 2 could cast the fusion hypothesis into doubt? I think common ancestry’s predictions are much less clear than you think they are.

But as you know my main argument regarding chromosomal fusion isn't that there is no evidence for chromosomal fusion. I'm willing to accept for the sake of argument that there is some evidence of fusion in human chromosome 2. My argument is thus the following: Even if human chromosome 2 does show evidence of a fusion event, at most all that would show is that current humans are descended from ancestors with 48 chromosomes. Whether those ancestors are basically human like you and me or whether they are apes is not addressed by the fusion evidence. But the fusion evidence tells us nothing about whether our lineage leads back to a common ancestor with apes (though it does reaffirm something we already knew--that humans have similar genetics to apes). Mainly, it just says that somewhere along the line that led to humans, there was a fusion event.

I'm just not seeing how, even when viewed in the most favorable light possible, the human chromosome 2 evidence is supposed to provide compelling evidence for human/ape common ancestry.

Thanks for writing.

Sincerely,

Casey

Bah, my mistake. At the end of my previous post, instead of "falsifiable data" I probably should have said "falsifiability."

Dear Jeremy,

Thanks for the good question. You asked: "But what about nonfunctional genetic similarities?" and rightly noted that I argued:

"Functional morphological and genetic similarities between humans and apes could be the result of common design just as much as common descent. That's a good principle to keep in mind as you investigate this issue: functional biological similarity is explained by common design just as well as it's explained by common descent."

A key word there is "functional," because I agree that nonfunctional similarities are better explained by unguided evolutionary processes. This shows the predictive power of intelligent design: ID predicts that structures will have function, so when we find non-functional structures (whether shared or not) those are not best explained by ID.

The problem for those who make the "nonfunctional genetic similarities" argument is that many examples of supposed shared "non-functional" similarities are turning out to be functional.

For example, you cited and linked to a paper titled "Evolution of the NANOG pseudogene family in the human and chimpanzee genomes," but yet there is evidence that many of these NANOG pseudogenes may in fact play functional roles. See J. Zhang et al., "NANOGP8 is a retrogene expressed in cancers," FEBS Journal, Vol. 273:1723-1730 (2006), which states:

"The expression of NANOGP8 in cancer cell lines and cancer tissues suggests that NANOGP8 may play important roles in tumorigenesis. This work not only has potential significance in stem cell and cancer research, but it also raises the possibility that some of the human pseudogenes may have regulatory functions."

Now I know that the NANOGP8 pseudogene is found only in humans, but one significant finding of the paper is that many of the other NANOG pseudogenes that are shared by humans and chimps (e.g. NANOG2, NANOG4, NANOG5, and NANOG7) were also found to be expressed in cancer cells (see Table 1). As the paper observed, "At the same time, other pseudogenes were found in OS732, HepG2 and MCF-7, while Nanog gene was also expressed in HepG2 and MCF-7." So suspicions of function for those shared pseudogenes may be equally valid as well.

So NANOG actually provides a good example of why it's a dangerous argument to argue or even tentatively conclude that shared pseudogenes are necessarily non-functional, largely because the data is pointing in another direction. As one paper from Annual Review of Genetics states: "pseudogenes that have been suitably investigated often exhibit functional roles." (Evgeniy S. Balakirev, and Francisco J. Ayala, Pseudogenes, "Are They "Junk" or Functional DNA?," Annual Review of Genetics, Vol. 37:123-51 (2003).)

Since 2003, the evidence for functions in pseudogenes has grown only stronger, as a recent 2011 paper in the journal RNA states:

Pseudogenes have long been labeled as "junk" DNA, failed copies of genes that arise during the evolution of genomes. However, recent results are challenging this moniker; indeed, some pseudogenes appear to harbor the potential to regulate their protein-coding cousins. Far from being silent relics, many pseudogenes are transcribed into RNA, some exhibiting a tissue-specific pattern of activation. Pseudogene transcripts can be processed into short interfering RNAs that regulate coding genes through the RNAi pathway. In another remarkable discovery, it has been shown that pseudogenes are capable of regulating tumor suppressors and oncogenes by acting as microRNA decoys. The finding that pseudogenes are often deregulated during cancer progression warrants further investigation into the true extent of pseudogene function. In this review, we describe the ways in which pseudogenes exert their effect on coding genes and explore the role of pseudogenes in the increasingly complex web of noncoding RNA that contributes to normal cellular regulation.

(Charles et al., "Pseudogenes: Pseudo-functional or key regulators in health and disease?," RNA, Vol. 17:792-798 (2011).)

In The Myth of Junk DNA, Jonathan Wells explains how pseudogenes can perform functions even if they are transcribed into RNA, but not translated into protein:

Since the sequence of DNA in a processed pseudogene is very similar to the sequence of the protein-coding segments (exons) of the complete gene, its RNA mirrors a messenger RNA transcribed from the functional gene, minus its introns. So (in the absence of alternative splicing) the RNA transcribed from one strand of the pseudogene is complementary to the messenger RNA transcribed from the opposite strand of the functional gene.

The two RNAs could bind together, much as the two complementary strands of DNA bind to each other. The result would be doublestranded RNA. But double-stranded RNA is not translated; instead, it interferes with translation and thereby reduces gene expression. Cells make good use of RNA interference to regulate the amount of protein they produce.

(Jonathan Wells, The Myth of Junk DNA pp. 50-51 (Discovery Institute Press, 2011) (internal citations removed).)

So there are good reasons to understand why these NANOG pseudogenes could have function, and in fact much evidence suggests they do have, as the FEBS Journal paper suggests, "regulatory functions."

In closing, you asked: "How can ID-friendly researchers use the principle of common design to make predictions about shared nonfunctional genetic similarities?"

In my opinion and experience, I think the principle of common design should lead ID-friendly researchers to be skeptical of claims that shared genetic similarities are non-functional. Too much data is pointing in the opposite direction.

Perhaps some shared genetic similarities will turn out to be functional. Perhaps some won't. But it's far too early to claim they don't have function.

ID doesn't claim that there is no common descent, nor does it claim that unguided evolutionary processes cannot be at work rendering some structures non-functional. But we should definitely take a wait-and-see approach and carefully consider what an ID-paradigm would say, because it implies we will discover much function.

Thanks again for the good question.

Sincerely,

Casey

p.s. the paper you cited doesn't discuss endogenous retroviruses, but since you mentioned them, it's worth noting that they too have been found to have evidence of function, and their distribution does not always fit the standard phylogeny. For details, see here, here, here, here, here, or here.

Before we mapped the human and chimp genomes we knew that the number of chromosomes differed b/w the two species. This fact represented a potentially huge problem for common ancestry, but just as predicted, a fusion point was discovered.

So let's compare the explanatory power of common ancestry vs. ID (the Jonathan Wells kind) in light of this data. Consider the following possible outcomes:

(1) After mapping the genomes and searching extensively, nothing resembling a fusion point is ever discovered
(2) A fusion point is discovered in our genome, which perfectly corresponds to two chromosomes from the chimp genome

The implications of (1) and (2) for common ancestry could be stated as follows:

(1) Common ancestry is in serious trouble.
(2) Common ancestry withstands yet another falsifying test and is verified once again.

Meanwhile, the implications for ID (the Jonathan Wells kind) could be stated as follows:

(1) Ha! Evidence against common ancestry! That's the way the designer did it!
(2) Ha! Evidence for common design! That's the way the designer did it!

Forgive me if I'm being a bit facetious, but my point should be clear: falsifiable data is where it's at. Like numerous other data, the chromosome 2 fusion is explained beautifully by common ancestry... not so much by ID (the Jonathan Wells kind).

Hi Casey-

In your post, you assert that functional genetic similarities could be explained by common design just as well as they are explained by common descent. For the time being, I am willing to accept that assertion at face value.

But what about nonfunctional genetic similarities?

Common ancestry both explains and predicts the existence of shared nonfunctional genetic elements such as retroelements, endogenous retroviruses, unitary pseudogenes, duplication pseudogenes, and retropseudogenes in related species. Here's a paper that provides some examples of such predictions.

How does the principle of "common design" explain this data? I know that most ID advocates argue that so-called "junk" DNA actually has some type of yet-to-be-determined function. But can a positive argument be made here?

You claim that human/ape common ancestry is compatible with ID, so I'd be interested in your answer to the following question: How can ID-friendly researchers use the principle of common design to make predictions about shared nonfunctional genetic similarities?

Cheers.

I believe as more is learned about junk DNA, we may have a much better idea of 'species specific' differences that should more clearly differentiate the genome of man and ape.

note:

On Not Reading Signature in the Cell: A Response to Francisco Ayala - Stephen Meyer
excerpt:,,, and (5) provide sites for Adenine-to-Inosine RNA editing, a function that is essential for both human development and species-specific brain development (Walters et al., 2009).,,,
http://www.stephencmeyer.org/news/2010/03/_this_is_part_2.html