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Professor Larry Moran poses five questions for the ID movement

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In a recent post over at his Sandwalk blog, Professor Larry Moran has been attempting to set the cat among the pigeons, with a list of five issues which, he anticipates, will lead to bitter recriminations within the “big tent” of the Intelligent Design movement.

Professor Moran is shocked, shocked, that Intelligent Design advocates sometimes publicly disagree on certain issues, as illustrated by a recent series of posts (by Sal Cordova, Dr. Branko Kozulic and myself) on the neutral theory of evolution. He writes:

The reason why this is so remarkable is that it almost never happens under the creationist big tent. Different Intelligent Design Creationists have widely conflicting views ranging from Young Earth Creationism to Theistic Evolution Creationism but they always manage to cover up those conflicts and present a united front in attacking evolution….

So, here’s the situation. If the IDiots actually start understanding modern evolution then there will be consequences. Some of them realize the implications and they are not happy. Here’s a brief list of issues that are now on the table under the big tent.

1. Darwinism: If the Idiots have been misinformed about evolution, which they have, then who is responsible and why were they misled by so many of their leaders?

2. Social Darwinism: If evolutionary biologists really believe in Neutral Theory and random genetic drift then how can they be supporters of the evil consequences of nineteenth century Darwinism? What about all those posts where evolutionary biologists were compared to eugenicists, racists, and Nazis?

3. Common Descent: This is a biggy. If Sal Cordova and the evolutionary biologists are right about the sequence differences between humans and chimpanzees, then it must mean that humans and chimps share a common ancestor. There will be no room under the big tent for Young Earth Creationists.

4. Junk DNA: If Cordova is right then most of the stochastic substitutions in the human genome are neutral. This must mean that most of our genome is junk. Oops! That won’t sit well with many creationists.

5. Theistic Evolution: There’s only one group that’s more evil than materialistic scientists and that’s theistic evolutionists. They are traitors. But if the IDiots actually were to accept the fundamental concepts of evolution, as Sal Cordova and Vincent Torley seem to be doing, then where does that leave Theistic Evolution Creationism? This cold be embarrassing when you look at all the posts on Uncommon Descent where theistic evolutionists have been mercilessly attacked.

Before I continue, I’d just like to point out something: the recent lively exchange of views between Intelligent Design advocates who have been blogging on Uncommon Descent on the subject of the neutral theory of evolution, has been carried out in a polite and cordial fashion, without even a trace of the name-calling, sarcasm and vulgarity that one so often finds at Websites run by outspoken atheists. That should tell you something.

I’d now like to address Professor Moran’s five questions, in turn.

1. Darwinism

1. Darwinism: If the Idiots have been misinformed about evolution, which they have, then who is responsible and why were they misled by so many of their leaders?

Professor Moran is assuming here that Intelligent Design advocates are more misinformed than most people, regarding what modern biologists believe about evolution. On this point, I think he is mistaken: nearly everyone who isn’t a biologist shares the same set of misconceptions.

A typical layperson’s view of evolution: E = NS acting on RV

In a recent post titled, Both wrong (13 February 2014), Professor PZ Myers referred to the view that “evolution is primarily a consequence of natural selection” as “a factually incorrect assertion.” Quite a few of his regular readers were sorely perplexed by this statement, and wrote in to say so:

Okay, so what am i missing? (Apart from a formal education in the biological sciences.)

I know (a little) about random mutations, the founder effect, & genetic drift. Aren’t they what natural selection acts upon? If so, it looks to me as though evolution is primarily a consequence of natural selection. (Dick the Damned)

How is evolution NOT a result of natural selection? Isn’t that exactly what Darwin taught? I am completely surprised and confused now. (dalehusband)

*Meekly raises hand*

I was under the (evidently mistaken) impression that, in nature, evolution is primarily driven by natural selection? (Sven)

I’m waiting for PZ to explain hisself here, but if he doesn’t do so soon I’m going to have to do it myself… and nobody wants that. (ChasCPeterson)

If certain lay Intelligent Design advocates such as myself, have (like most laypeople) been misinformed as to what modern biologists believe about evolution, it certainly isn’t because they were misled by leading figures in the Intelligent Design movement.

Natural selection dominates media and Internet coverage of evolution

One significant reason for the widespread confusion among laypeople is the fact that science bloggers write a lot more frequently about natural selection than about genetic drift – a point which was astutely made by commenter John Harshman, who wrote:

Well, I’m a bit surprised at the comments. Apparently Larry Moran was right, and most people have no idea about the prevalence of neutral evolution. But I can see why. Who writes popular books on the glories of drift? All the cool stuff — flight, big sharp teeth, fancy ornaments, tool use, etc. — is selection. All the science blogs are full of bizarre adaptations, but seldom a word about the boring, pointless bulk of fixations. Junk DNA just isn’t as much fun, even for many biologists, which is why so many are trying to kill it off.

The most vocal leading scientists who popularize evolution are neo-Darwinians

The other main reason why laypeople (including myself) have been misled regarding what evolutionary biologists currently believe about evolution, is that a small but vocal minority of biologists continue to espouse the neo-Darwinian view. The following quote by Richard Dawkins is typical of those scientists who fall into this camp:

There is one particular property of living things, however, that I want to single out as explicable only by Darwinian selection. This property is the one that has been the recurring topic of this book: adaptive complexity. (The Blind Watchmaker, New York: W. W. Norton & Company, Inc., 1986, Chapter 11, “Doomed Rivals,” p. 288.)

In the book’s preface, Dawkins states that he wrote the book “to persuade the reader, not just that the Darwinian world-view happens to be true, but that it is the only known theory that could, in principle, solve the mystery of our existence.”

Dawkins is not the only vocal defender of natural selection. Here’s a short passage, taken from a post titled James Shapiro goes after natural selection again (twice) on HuffPo (22 August 2012) by evolutionary biologist Jerry Coyne, in which he roundly declares that modern evolutionary biologists regard natural selection as “the only game in town” when it comes to explaining adaptations, and criticizes biologist James Shapiro for thinking otherwise:

How on earth do cytogenetics or molecular genetics alone explain the transformation of fish into tetrapods, deerlike animals into whales, or account for cryptic coloration, mimicry, and adaptive behaviors? They can’t, for there has to be some process that winnows out the variation that arises. That process is natural selection…

I wouldn’t go after Shapiro except that he spews this anti-evolutionary nonsense at HuffPo, and naive readers might get the impression that biologists are beginning to doubt that natural selection is important. Well, as far as evolutionary biologists regard adaptations, it is: natural selection is the only game in town.

Yes, we now know of a whole host of new mechanisms to generate genetic variation, including symbiosis and the ingestion of DNA from distantly related species. But to produce adaptation, something has to winnow out the wheat from the chaff: those variants that reduce reproduction from those that enhance it. And that’s natural selection. There is no alternative, and Shapiro, despite his endless series of “blogs,” has never suggested one.

How I gradually came to realize that evolutionary biologists aren’t neo-Darwinians anymore

Gradually, however, I came to realize that Coyne’s views were no longer typical of modern evolutionary biologists. I had previously written about the views of a few dissenting biologists back in 2012, in a post titled, Larry Morgan defends Paul Nelson! (December 11, 2012). But I still imagined them to be representing the views of a beleaguered minority of scientists in the field. It was only recently that I became aware that this “beleaguered minority” was actually a majority!

What prompted this startling realization was the publication of a couple of recent posts by prominent evolutionary biologists PZ Myers (The state of modern evolutionary theory may not be what you think it is, 14 February 2014) and Larry Moran (On the difference between Neutral Theory and random genetic drift, 15 February 2014). In his post, PZ Myers summed up the findings of science over the last few decades as follows:

First thing you have to know: the revolution is over. Neutral and nearly neutral theory won. The neutral theory states that most of the variation found in evolutionary lineages is a product of random genetic drift. Nearly neutral theory is an expansion of that idea that basically says that even slightly advantageous or deleterious mutations will escape selection — they’ll be overwhelmed by effects dependent on population size. This does not in any way imply that selection is unimportant, but only that most molecular differences will not be a product of adaptive, selective changes.

Professor Moran concurred:

What Neutral Theory tells us is that a huge number of mutations are neutral and there are far more neutral mutations fixed by random genetic drift that there are beneficial mutations fixed by natural selection. The conclusion is inescapable. Random genetic drift is, by far, the dominant mechanism of evolution.…

The revolution is over and strict Darwinism lost. We now know that random genetic drift is an important mechanism of evolution and there’s more to evolution than natural selection. Unfortunately, this blatantly obvious fact is not understood by the vast majority of people and teachers. There are even many scientists who don’t understand evolution.

There was more. Professors PZ Myers and Larry Moran also argued that a non-Darwinian mechanism could account for the origin of most complex structures in living things. In a post entitled, Complexity is not usually the product of selection (11 December 2012), PZ Myers forthrightly declared:

I think if selection were always the rule, then we’d never have evolved beyond prokaryotes — all that fancy stuff eukaryotes added just gets in the way of the one true business of evolution, reproduction…

The bottom line is that you cannot easily explain most increases in complexity with adaptationist rationales. You have to consider chance as far more important, and far more likely to produced elaborations…

Even in something as specific as the physiological function of a biochemical pathway, adaptation isn’t the complete answer, and evolution relies on neutral or nearly neutral precursor events to produce greater functional complexity.

Professor Larry Moran subsequently endorsed P.Z.Myers’ article, in a post of his own, entitled, On the Evolution of Complexity (11 December 2012), in which he wrote:

Can you go from some simple character to a more complex feature without invoking natural selection? Yes, you can. Complex features can evolve by nonadaptive means. Just think of our complex genome and read The Origins of Genome Architecture by Michael Lynch.

Want a more simple example? Read the latest post by PZ Myers: [αEP: Complexity is not usually the product of selection]1.

This is an important point. You can’t just assume, without question, that a complex trait must be an adaptation and must have arisen by natural selection. That applies to molecular complexes and also to complex behavior.

These posts, coupled with the two February 2014 posts by Professors Myers and Moran on the triumph of the neutral theory, made me decide that the time had come to stop going after neo-Darwinian evolution, as most biologists no longer accepted it anyway, and focus instead on the neutral theory of evolution. This is what I attempted to do in my first post on the neutral theory. My decision to focus on fixation rates turned out to be tactically unwise, and the factual errors that Professor Moran subsequently exposed in my post proved to be a valuable learning experience for me. But my intention – which was to shift the focus of attack away from neo-Darwinism and direct it at modern-day versions of evolution – was, I believe, quite right.

2. Social Darwinism

2. Social Darwinism: If evolutionary biologists really believe in Neutral Theory and random genetic drift then how can they be supporters of the evil consequences of nineteenth century Darwinism? What about all those posts where evolutionary biologists were compared to eugenicists, racists, and Nazis?

The Uncommon Descent posts on Social Darwinism highlighted the enormous harm wrought by three central ideas that were actively promulgated by nineteenth-century evolutionists: first, the denial of the human soul; second, the assertion that our every act (leaving aside random quantum fluctuations which cannot truly be called actions) is determined by circumstances beyond our control, which takes away our freedom of choice; and finally, the progressivist accounts of evolution that were widely propagated not only by Haeckel but also by Darwin himself, as I’ve documented in my post, Rewriting history: Can a Darwinist believe in the scala naturae? (Darwin did.) and Darwin, Kingsley, evolution and racism. (Good arguments for the existence of an immaterial human soul can be found here and here; see also here, here and here. For a refutation of arguments that the scientific evidence for determinism is so strong as to preclude the possibility of free will, see here and here; see also here, here and here.) The first two ideas debased people’s view of what it means to be human, causing many people to think of themselves as mere “meat machines” instead of individuals made in the image and likeness of God, their Creator; while the third idea lent a new legitimacy to scientific racism (which had first appeared back in the eighteenth century), as some races were thought to occupy a much higher place on the evolutionary ladder than others.

The first two ideas continue to poison people’s minds, and the neutral theory of evolution is just as imbued with them as neo-Darwinism is.

Professor Moran might point out that progressivist models of evolution are badly flawed, and that contemporary biologists unanimously reject racism. But he might do well to ponder Stephen Jay Gould’s dictum that human equality is a contingent fact of history. From a materialist standpoint, this is surely correct: were the Neandertals or Denisovans alive today, I doubt whether most evolutionary biologists would regard them as their moral equals, with the same rights to life, liberty and the pursuit of happiness as we currently enjoy.

3. Common Descent

3. Common Descent: This is a biggy. If Sal Cordova and the evolutionary biologists are right about the sequence differences between humans and chimpanzees, then it must mean that humans and chimps share a common ancestor. There will be no room under the big tent for Young Earth Creationists.

Hold on a second, Professor Moran! First of all, lumping Sal Cordova in with “evolutionary biologists” is a bit of a joke, as Sal is a committed young-earth creationist. Second, Sal Cordova is well aware of the genetic similarities and differences between humans and chimpanzees, and some time ago, he wrote a carefully worded post (which Moran reviewed), in which he drew a distinction between physical ancestors and what he called “conceptual ancestors,” and went on to argue that extensive physical similarities between two species of organisms did not mean that they were related. Third, Sal has recently written a post titled, Larry almost got it right, but he just can’t turn the corner (17 April 2014), in which he elucidates his views on the genetic differences between humans and chimpanzees, and on the neutral theory of evolution.

For my part, I have made no secret of my belief in the common descent of organisms. But if someone in the Intelligent Design movement thinks they can explain the genetic similarities and differences between humans and chimps without postulating a common ancestor for these two primates, then all I can say is: good luck to them. Why is that? Because in the ultimate scheme of things, I don’t see the question of whether we’re related to chimps as a very important one. Nothing really hangs on it, in terms of the way we live our lives. At the very most, the discovery might bring limited medical benefits, which Professor Jerry Coyne summarizes in a post titled, Of what value is evolutionary biology in medicine? (3 April 2009).

Far more important, however, than the historical question of whether we share a common ancestor with the chimp is the more fundamental philosophical question: are the genetic differences between humans and chimps at least partly the result of an act of intelligent design, or are they entirely caused by unguided processes? In a future post, I hope to outline my reasons for believing that intelligent design is the best explanation for some of the major differences between humans and other primates.

In short: the Intelligent Design “big tent” remains standing. In order to see why it’s still standing, Professor Moran just needs to get his philosophical priorities straight.

4. Junk DNA

4. Junk DNA: If Cordova is right then most of the stochastic substitutions in the human genome are neutral. This must mean that most of our genome is junk. Oops! That won’t sit well with many creationists.

Sal Cordova has already responded to Professor Moran’s argument in the post I mentioned above. I’d like to make a few comments of my own.

It appears to me that Professor Moran’s reasoning is faulty on two counts. First, the fact that “most of the stochastic substitutions in the human genome are neutral” doesn’t imply that the sections of the human genome in which they occur serve no function. It simply means that the (mostly neutral) changes taking place in that section of the genome will neither help nor harm the organism. By itself, that tells us nothing about what percentage of the genome is junk.

Second, Professor Moran is committing a verbal sleight-of-hand here: he is equating “neutral” with “junk.” As Professor Moran himself writes: “The correct definition of ‘junk’ is DNA that has no known function.” Note the wording here: “no known function.” A neutral mutation, on the other hand, is simply one that does not affect an organism’s ability to survive and reproduce. That doesn’t mean the mutation has no function; it simply means that it has no present function. A neutral mutation that might not affect an organism’s ability to reproduce, but it could still conceivably have an impact (positive or negative) on the fertility of the organism’s distant descendants. Or again, the mutation might (for all we know) incorporate information that is of no use to the particular species of organism in which it occurs, but which eventually turns out to be useful to that species’ evolutionary descendants. Of course, one would want to see some experimental evidence for these scenarios. The reason why I’m mentioning them is simply to show that Professor Moran’s equation of “neutral” with “junk” is conceptually careless.

Junk DNA – how much is there?

I’d like to preface my remarks by saying that I have no expertise whatsoever in genetics, and my knowledge of junk DNA is very limited. However, I’ve watched Professor PZ Myers’ video on junk DNA, and I’ve also skimmed Professor Moran’s lengthy review of Dr. Jonathan Wells’ book, The Myth of Junk DNA (see here for some more positive reviews and here for a list of news updates on junk DNA, over at Evolution News and Views). Suffice it to say that when a Professor of Medical Genetics writes, “I strongly recommend The Myth of Junk DNA, a lucid account of the evidence that junk DNA has many diverse biological functions,” and when a Professor of Microbial Genetics and Cell Biology adds that “Jonathan Wells has clearly done his homework,” you know the book can’t be as awful as Professor Moran claims it is. A short summary of Dr. Wells’ views on junk DNA can be found in his online article, Not Junk After All: Non-Protein-Coding DNA Carries Extensive Biological Information.

I would also recommend reading Dr. Richard Sternberg’s article, Matheson’s Intron Fairy Tale, Professor Moran’s reply, Sternberg’s counter-reply, Moran’s second response to Sternberg, and the follow-up article by Dr. Jonathan Wells, titled, The Fact-Free “Science” of Matheson, Hunt and Moran: Ridicule Instead of Reason, Authority Instead of Evidence. The upshot of this discussion is that of the number of human introns (non-protein coding parts of genes) that undergo alternative splicing (which suggests that they have a biological function) is at least 45,000, out of 190,000 introns in the human genome – which is far more than the figure of up to 1,000 that was originally estimated by Matheson, but which may still represent less than 30% of all introns. In short: the question of junk DNA remains open.

Of more recent interest is the September 2012 announcement by the leader of the ENCODE team that 80 percent of the genome has a “biochemical function,” meaning that “It’s not junk.” (Birney has blogged about his announcement here and here. In a review article for Nature, titled, Fighting abut ENCODE and junk (Nature News blog, 6 September 2012), science correspondent Brendan Maher offers a cooler assessment:

…[P]erhaps the main conclusion should have been that 20% of the genome in some situation can directly influence gene expression and phenotype of at least one human cell type. It’s a far cry from 80%, but a substantial increase from 1%.

Science writer Ed Yong (who originally broke news of ENCODE’s discovery), summarizes the ongoing controversy in an addendum to his report in Discover magazine (5 September 2012; update 7 September 2012):

Birney was right about the scepticism. [T. Ryan] Gregory [from Guelph University] says, “80 percent is the figure only if your definition is so loose as to be all but meaningless.” Larry Moran from the University of Toronto adds, “Functional” simply means a little bit of DNA that’s been identified in an assay of some sort or another. That’s a remarkably silly definition of function and if you’re using it to discount junk DNA it’s downright disingenuous.”…

Gregory asks why, if ENCODE is right and our genome is full of functional elements, does an onion have around five times as much non-coding DNA as we do? Or why pufferfishes can get by with just a tenth as much? Birney says the onion test is silly. While many genomes have a tight grip upon their repetitive jumping DNA, many plants seem to have relaxed that control. Consequently, their genomes have bloated in size (bolstered by the occasional mass doubling)… Conversely, the pufferfish has maintained an incredibly tight rein upon its jumping sequences. “Its genome management is pretty much perfect,” says Birney. Hence: the smaller genome.

But Gregory thinks that these answers are a dodge. “I would still like Birney to answer the question. How is it that humans “need” 100% of their non-coding DNA, but a pufferfish does fine with 1/10 as much [and] a salamander has at least 4 times as much?”

Regarding the onion test, readers might be interested in having a look at Professor Larry Moran’s post in response to a post by Jonathan M., and Jonathan M.’s subsequent reply to Moran, titled, Why the “Onion Test” Fails as an Argument for “Junk DNA” (2 November 2011). Professor Moran’s brief response is here.

Professor Moran, who still thinks that 90% of our DNA is junk, also makes the telling point that “almost 50% of our genome is littered with dead transposons and bits of transposons,” which one would not expect to have a function. Yet even he acknowledges that “there are some other scientists who think that all of the human genome is functional.”

In light of the above-mentioned uncertainties, I think a prudent estimate of the percentage of junk DNA in the human genome would be: somewhere around 50%. It could be quite a bit more … or it could be a lot less.

Junk DNA – how much could the Intelligent Design movement live with?

Suppose that the “50% junk” figure is true. Could the Intelligent Design movement live with that? Personally, I don’t see why not. Let’s try a little thought experiment. Would it bother you if 1% of our genome turned out to be junk? I don’t imagine so. All right. What about 10%? That still leaves 90% that is functional, so I can’t see why it would matter either. Well, what about 50%? Even if 50% of our DNA were junk, you could still say that half of the human genome is there for a reason, and that the remaining half, while non-functional, isn’t harming us. That doesn’t sound so bad to me. What’s the problem?

Professor PZ Myers, in a talk given to Skepticon IV on November 19-20, 2011, quotes [at 4:56] a well-known passage from the writings of Professor William Dembski on junk DNA:

[Intelligent] design is not a science stopper. Indeed, design can foster enquiry where traditional evolutionary approaches obstruct it. Consider the term “junk DNA.” Implicit in this term is the view that because the genome of an organism has been cobbled together through a long, undirected evolutionary process, the genome is a patchwork of which only limited portions are essential to the organism. Thus on an evolutionary view we expect a lot of useless DNA. If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit function.
(“Science and Religion” in First Things, 17 March 2009.)

As far as I can tell, all that follows from the hypothesis of Intelligent Design is that any organisms that were designed de novo, or from scratch, should be free of junk DNA. But even if the Intelligent Designer subsequently manipulated the DNA of these organisms’ descendants, to make other kinds of organisms, I see no reason to suppose that He would have also “wiped the slate clean” at the same time, and erased all traces of the junk DNA that had accumulated in that organism over the course of time. Of course, a Designer might do that, as an act of courtesy; but who is to say that He must? Why not simply let the junk stay there, if it’s not harming the organism and if it’s not likely to harm its descendants? What do readers think?

Dr. Richard Sternberg on letting God be God

In a 2008 article titled, How My Views on Evolution Evolved, Dr. Richard Sternberg writes:

I cannot overemphasize the number of times I have listened to evolutionary biologists theologize on the basis of some gnosis they have concerning divine actions. One case stands out in particular. Francis Collins, director of the National Human Genome Research Institute at the NIH, showed a small group that included me a presumably “dead gene,” a pseudogene. Now his line of argumentation went something like this:

A. We know this pseudogene has no function, and therefore no purpose.

B. We know also that God would not make functionless, purposeless objects.

Therefore God had no role in the creation of the pseudogene – it was a random event.

Based on my conversations with Collins, it became apparent to me that his god is a strict nineteenth-century utilitarian who would, if he deigned to create, manufacture only highly efficient and minimalist entities. His deity would only provide evidence of his handiwork by means of Bauhaus-like architectures, as Baroque or Rococo designs would be, well, excessive and wasteful. A purposefully, intelligently designed cell would, judging from his points, resemble ever so much Fritz Lang’s Metropolis. And since what we so often observe are over-the-top excrescences and strings of DNA that just don’t seem to have a purpose – bad, sloppy design according to Collins’ way of thinking – we know, we know – as a scientific fact, no less – that the genome is randomly cobbled together in length and breadth and all the way up and down.

It seems to me that Dr. Sternberg has a valid point here. It is presumptuous for us to assume that God would not allow any junk in the human genome. That being the case, we should be wary of predicting the occurrence of little or no junk DNA in the genome.

I’d now like to address Professor Larry Moran’s final point.

5. Theistic Evolution

5. Theistic Evolution: There’s only one group that’s more evil than materialistic scientists and that’s theistic evolutionists. They are traitors. But if the IDiots actually were to accept the fundamental concepts of evolution, as Sal Cordova and Vincent Torley seem to be doing, then where does that leave Theistic Evolution Creationism? This cold be embarrassing when you look at all the posts on Uncommon Descent where theistic evolutionists have been mercilessly attacked.

The term “Intelligent Design proponent” could be understood in a very broad sense, as including anyone who believes that the cosmos (or at the very least, some feature of it) was designed by an Intelligent Being. On this broad definition (used by Professor Michael Behe below), theistic evolutionists already qualify as Intelligent Design advocates.

However there are two major differences separating the ID and theistic evolution camps. As regards science, the critical question that separates Intelligent Design proponents from theistic evolutionists is not whether evolution occurred, nor even whether evolution (if it occurred) was guided by God, but rather, whether the existence of an Intelligent Being guiding evolution is scientifically detectable. Modern-day theistic evolutionists say no; Intelligent Design advocates say yes.

In addition, theistic evolutionists and ID advocates are also divided on a theological level. In a 2007 post titled, Kenneth R. Miller and the Problem of Evil, Part 2 (25 October 2007), Intelligent Design advocate Professor Michael Behe gives a very clear exposition of the key issues that separate him from Catholic biochemist Kenneth Miller, who like Behe accepts common descent but rejects Intelligent Design. Although he dislikes the label, Miller could fairly be described as a theistic evolutionist. At the end of Part 1 (October 24, 2007) of his series of posts, Behe had written:

So let me emphasize: Kenneth Miller is an intelligent design proponent. He believes that the laws of the universe were purposely set up to permit life to develop. Miller thinks that, to accomplish the goal of life, the universe had to be designed to the depth of its fundamental physical constants. I agree with him as far as he goes, but, on the other hand, as I write in The Edge of Evolution, I think design extends further into the universe, past physical constants, past anthropic coincidences, and well into biology. Yet, with respect to design, he and I differ only on degree, not on principle.

In Part 2, Behe continues:

Let me emphasize the last point of my previous post: Miller and I are only quibbling over the extent of design in the universe. The fact of design, the principle of design, we agree on.

Now, let’s look a little closer at where Ken Miller draws the limits of design (the edge of evolution, one might say). Although they are clearly necessary, is there reason to suppose that the bare laws and constants of the universe — even if properly tuned — are sufficient to assure life occurs in our universe, as Miller supposes? The answer is no — many other features than just the bare laws of the universe have to be gotten right. I discuss this at considerable length in the last chapter of the book. But don’t just take my word for it. The prominent bioinformatician Eugene Koonin recently published a paper entitled “The cosmological model of eternal inflation and the transition from chance to biological evolution in the history of life”, (Biol Direct., 2007, 2:15). The gist of the paper is that — even given fine tuned laws and constants — the origin of life in our universe is so unlikely, that the non-theist Koonin invokes an infinite multiverse to assure that life happens somewhere.

…So suppose Koonin is right that fine tuning the laws of the universe is far from sufficient to assure life. In that case, switching to Miller’s scenario, God would have set up a generic universe whose laws and constants were necessary for life, but not sufficient. Since many other conditions are required for life, Miller’s God likely made a fine tuned universe for naught. It would likely be a finely tuned universe that’s nonetheless barren of life.

In The Edge of Evolution I agree with Miller (and other “theistic evolutionists”) that the laws and constants of our universe are fine tuned, but argue that “fine-tuning” extends much more deeply into nature than previously supposed, and actually extends into life itself, at least down to the level of vertebrate class. I cleverly call this view “extended fine-tuning.” In the book I argue that any person who accepts a theistic evolutionary view, such as Miller does, should have no trouble in principle with the extended fine tuning view. It is, after all, just a matter of degree. In either case the designer fine tuned enough details of our universe to get intelligent life to arise.

In Part 3 of his series, Professor Behe goes on to address the real reason that he thinks theistic evolutionists balk at Intelligent Design: since some organisms that harm human beings (e.g. the malaria parasite) appear to have been designed according to the criteria used by the ID movement, that would appear to imply that the Designer is malevolent. In other words, the issue dividing the two camps, as Behe sees it, is a theological one. Behe’s thoughtful reply is well worth reading. After adducing supporting quotations, Behe argues that Kenneth Miller and Francisco Ayala “embrace Darwinism, at least in large part, for theological reasons”: if God is not involved in the “nuts-and-bolts” of designing Nature, then He cannot be held responsible for its dangerous by-products (such as mosquitoes). Behe doesn’t buy this argument: “It seems to me that designing a poor Darwinian process that inevitably spins off natural evils leaves One as vulnerable to being sued for incompetence as directly designing them as finished products.” He goes on to say that “as a scientist, one is obliged to look at the evidence of nature dispassionately and nonjudgmentally.” Behe adds that for all we know, parasites and viruses may “actually play positive roles in the economy of biology, of which we are in large part unaware,” in which case the harm they cause to humans is an unintended side-effect. Finally, he points out that “[e]ven if God purposely designed the malarial parasite, He may not have decreed that a particular infected mosquito would bite a particular person on a particular day.”

Behe’s conclusion is worth quoting in full:

As I wrote in The Edge of Evolution, it seems to me that our world was designed to be a a dangerous living stage, one that’s set up for improvisational theater. It allows for real suffering, real pleasure, real pain, real joy. It allows for real freedom and real consequences. But if the world were not designed in sufficient detail, then no intelligent life would be around to act on the stage.

Comments
Considering the point 3 of the pr Larry Moran question, ".../...3. Common Descent: This is a biggy. If Sal Cordova and the evolutionary biologists are right about the sequence differences between humans and chimpanzees, then it must mean that humans and chimps share a common ancestor. There will be no room under the big tent for Young Earth Creationists..../..." I have to day sufficient consistent material, data and results to demonstrate - considering the chromosome4 - that this human chromosome is an exception and "out of continuity" comparing it with all other primates chromosomes4 and all 23 remaining human chromosomes: The 5 steps of my upcoming demonstration are: Phase 1 - Analysis of populations of codons: Correllations 99.99% of the genomes of humans and chimpanzees but emergence of two clusters of chromosomes highly differentiated (human chromosomes 16 17 19 20 and 22). Phase 2 - Evidence of a classification scale of the 24 human chromosomes (focusing particularly on the 2 extremal limit borders chromosome4 and chromosome 19). Phase 3 - The chromosome4: significant differentiations between primates (human, chimp, gorilla, oran utang). Phase 4 - The chromosome4: Meta-exclusive differentiation between humans and other primates (chimp, gorilla, oran utang). Phase 5 - chromosome4: Meta-exclusive differentiation vis-à-vis the other 23 human chromosomes.jean-claude perez
May 6, 2014
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Considering the point 3 of the pr Larry Moran question, I have to day sufficient consistent material, data and results to demonstrate - considering the chromosome4 - that this human chromosome is an exception and "out of continuity" comparing it with all other primates chromosomes4 and all 23 remaining human chromosomes: The 5 steps of my upcoming demonstration are: Phase 1 - Analysis of populations of codons: Correllations 99.99% of the genomes of humans and chimpanzees but emergence of two clusters of chromosomes highly differentiated (human chromosomes 16 17 19 20 and 22). Phase 2 - Evidence of a classification scale of the 24 human chromosomes (focusing particularly on the 2 extremal limit borders chromosome4 and chromosome 19). Phase 3 - The chromosome4: significant differentiations between primates (chimp, gorilla, oran utang). Phase 4 - The chromosome4: Meta-exclusive differentiation between humans and other primates (chimp, gorilla, oran utang). Phase 5 - chromosome4: Meta-exclusive differentiation vis-à-vis the other 23 human chromosomes.jean-claude perez
May 6, 2014
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Dears Pietr, Joe or Gordon, I'm sorry for your unapropried comments on SANDWALK of the Sal Cordova entry entitled Vodka! Jean Claude Perez, the golden ratio, dragon curve fractals and musical design in “junk DNA”... The reason is that all (ALL) their comments were done without reading the basic original article: I suggest you reading the original basic peer review article of 2010 published in Interdisciplinary Science: http://fr.scribd.com/doc/95641538/Codon-Populations-in-Single-stranded-Whole-Human-Genome-DNA-Are-Fractal-and-Fine-tuned-by-the-Golden-Ratio-1-618 and my 2013 peer review article: http://www.scirp.org/journal/PaperInformation.aspx?paperID=37457#.U2Mwlfl_trAjean-claude perez
May 1, 2014
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But that is not close, to resume: 1/ in my 2nd post, I show that distance between chimp and human is lower that generally considered: 99.99% 2/ but in my first post, I show great differenciation between human and monkeys... 3/ in https://plus.google.com/103572438711329205534/posts/26WczM9aQbS we show that Human chromosome4 has a typical property absent in all other species and particularly monkeys!jean-claude perez
April 30, 2014
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Mung #108: No. I did not say that. I paste again my statement: "No, because if either NS or design are important driving forces, then functional sequences expand and are fixed for reasons that have nothing to do with drift. After one sequence expands because it is functional, and not because of drift, then that sequence is relatively “conserved” because of its function. IOWs, drift can still act on the sequence, but only on those mutations that conserve the function." The idea is simple. If a sequence expands, is fixed and conserved because of its function, let's say by positive NS, (even if its origin is design), it is not fixed by genetic drift. IOWs, if we find some sequences which are fixed in a population, they could have been fixed: a) by drift b) by positive selection If a complex functional protein is generated by design, for example, it will expand and be fixed because it is functional, by positive selection, and not by drift. It is true that drift can act randomly both on neutral and on functional sequences, but most of random variation is neutral, s in practice drift act on neutral mutations, because functional random mutations are so rare that they are almost non existent. Designed functional variation certainly happens more often, but still it would be foolish to expect that it is fixed by drift, competing with the many neutral variations. Function originates by design and expands by positive selection.gpuccio
April 30, 2014
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then in the same time human and chimp whole genomes are >99% correlated at codon population: see: http://fr.scribd.com/doc/200161987/Why-Human-and-Chimp-whole-genomes-are-99-99-close-pdf and book codex biogenesis: http://www.amazon.co.uk/Codex-Biogenesis-harmonies-g%C3%A9nome-latome/dp/2874340448jean-claude perez
April 30, 2014
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Dear Pr Larry Moran here a step which coupld give progress in the comparaison human/chimp: "3. Common Descent: This is a biggy. If Sal Cordova and the evolutionary biologists are right about the sequence differences between humans and chimpanzees, then it must mean that humans and chimps share a common ancestor. There will be no room under the big tent for Young Earth Creationists." Please read: http://fr.scribd.com/doc/186894835/jcperezEvolutionFibonacciPrimatesChromosomes4UKjean-claude perez
April 30, 2014
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gpuccio:
Drift act randomly, therefore it should act mainly on neutral mutations.
Are you asserting that genetic drift only acts randomly on neutral mutations, but it does not act randomly on non-neutral mutations? If so, I suggest, humbly, that you do not understand genetic drift.Mung
April 26, 2014
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Mung: No, because if either NS or design are important driving forces, then functional sequences expand and are fixed for reasons that have nothing to do with drift. After one sequence expands because it is functional, and not because of drift, then that sequence is relatively "conserved" because of its function. IOWs, drift can still act on the sequence, but only on those mutations that conserve the function. So, if say half of the differences we observe between humans and chimps are functional, and have been fixed independently from drift (for example, because they were designed as functional and expanded by positive NS), then the number of mutations that expanded by random drift is half of what we would expect from the mutation rate. That's exactly what we would expect if a large part of non coding DNA in the ancestor of humans and chimps was already functional.gpuccio
April 26, 2014
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gpuccio:
Drift act randomly, therefore it should act mainly on neutral mutations.
But that is only because most mutations are neutral, correct? If most mutations were not neutral how would that impact or change genetic drift? My thinking is that it would not, because drift is about sampling and not about selection (or lack thereof). Am I making sense?Mung
April 26, 2014
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Mung: Drift act randomly, therefore it should act mainly on neutral mutations. It is possible, obviously, that random drift act on potentially functional mutations, which are treated as though they were neutral (IOWs in that context their potential function cannot be "recognized" by the process going on). Sal has emphasized that possibility many times, and I think he is right. The simple fact is that "positive" NS is practically non existent. The few cases we know of are very special cases, with simple variation (usually with reduction of the existing function) and casual advantage in very stressing environmental contexts (see antibiotic resistance). It's what we call "microevolution". On the other hand, "negative" selection (also called "purifying" selection) is IMO an nimportant process, which takes place all the time. Mutations which happen in a functional sequence are either deleterious (and therefore eliminated, more or less, by negative selection), or neutral, and therefore potentially able to be fixed by drift. Instead, mutations happening in non functional sequences are by definition neutral, because there is no function to be lost. That's why all mutations are neutral in non functional sequences, and the number of mutations that are fixed in that kind of sequences should be related to the total number of mutations. On the contrary, in functional sequences, some mutations are neutral and some are deleterious. Therefore, the total number of neutral mutations in that kind of sequence will be lower, and therefore not connected to the mutation rate. This is the basis of Moran's argument. As you can see, the flaw of that argument is that it does not take into account the number of functional mutations. Now, they believe that those functional mutations are due to positive selection (yes, even neutralists in the end believe that). That is essentially impossible. We believe those functional mutations are designed. However, in both cases, the functional mutations will not behave like neutral mutations, and therefore Moran's argument is wrong.gpuccio
April 26, 2014
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Mung: Errata corrige: it's non coding DNA, not non coding DNS. Too much internet culture, I suppose. :)gpuccio
April 25, 2014
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Mung: Those are the total mutations that happened (if the number is right). They could in principle be any kind of mutation: neutral, positively selected, or designed. Moran argues that they must be almost all neutral, because the number corresponds (more or less) to how many neutral mutations would be fixed by drift if the non coding DNS were really non functional, and therefore non affected by negative selection. I argue that he is ignoring that at least part of those mutations must be functional (we are different from chimps, and better at least for some tasks :) ), and that the number of functional mutations, which I called X, could well be great. It must be subtracted from the number of true neutral mutations. Therefore: a) X mutations are functional, and can be explained only by design. b) 22.4 million - X mutations are neutral and fixed by drift. c) If X is great, the total number of neutral mutations no more corresponds to what would be (more or less) expected by the mutation rate.. It is definitely lower. d) Therefore, non coding DNA is functional, and is affected by negative selection. QED.gpuccio
April 25, 2014
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gpuccio:
Larry Moran, in his original post at Sandwalk, which in some way is the origin of all this discussion, states that according to series of reasonable assumptions the number of fixed mutations in humans since they diverged about five million years ago from chimps is of about 22.4 million.
So, are the mutations neutral or not, or does it even matter? I keep hoping kairosfocus will weigh in, as he seems to understand sampling. Wikipedia:
Genetic drift or allelic drift is the change in the frequency of a gene variant (allele) in a population due to random sampling.
Is that random sampling based upon the neutrality or non-neutrality of the allele? If it were, it would not be random. Am I wrong?Mung
April 24, 2014
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wd400 and Mung: I will try another time, in name of a discussion which for me too has been interesting. Let's start from the beginning. Larry Moran, in his original post at Sandwalk, which in some way is the origin of all this discussion, states that according to series of reasonable assumptions the number of fixed mutations in humans since they diverged about five million years ago from chimps is of about 22.4 million. I will accept that, but I want to clarify that it is only a gross estimate, which depend critically on assumptions which have a wide margin of error. OK, the second step is that, according to the neutralist theory, about 130 mutations per generation are expected in humans. Again, that is a wide approximation. The numbers on which that is bases can certainly be somewhat different than assumed. Finally, by other computations, again depending on reasonable, but not necessarily exact, assumptions, the number of mutations assumed in humans (22.4 million) "corresponds to a substitution rate (fixation) of 121 mutations per generation and that's very close to the mutation rate as predicted by evolutionary theory". (Larry Moran's words) Well, this is the argument. I have already argue that, first of all, this is not an exact expectation. It is gross, and is based on many assumed numbers which can be tweaked as we like, and have wide margin of errors, which would strongly influence the "amazing coincidence" (again Larry Moran's words). It is strange how non design theorists become suddenly sensible to "coincidences" sometimes, while utterly ignoring probabilistic arguments when they come from ID theorists. Oh, that's probably human nature, after all. :) That said, I would like to ask wd400 a few simple questions starting from that model. 1) Do you admit that there are important functional differences between humans and chimps? 2) If that is the case (I would say it is), do you realize that, if we admit for the moment that those differences are related to modifications in the genome (let's ignore for the moment the role of epigenetic transmission of information), then you are computing in those 22.4 million mutations, also the functional mutations. 3) Now, I will assume (we can assume too!) that the functional mutations, whatever their number, are not the result of neutral mutations (that would really be an "amazing coincidence"). They can be designed, as I believe, or they can be the result of positive selection (the old neo darwinian explanation). But simple random variation cannot certainly explain them. 4) Now I ask you: how many mutations, according to you, are responsible of the functional novelties in humans? I suppose you don't know, and I don't know either. But I care about that aspect, while you seem not to care. Beware, that number could be small, but it could be big. Let's say, for the moment, let's call that number X. 5) Therefore, we must subtract the number X from our 22.4 million mutations. The result will be the real number of neutral mutations that have been fixed by drift. 6) Then, we need to know how those 22.4 million mutations are distributed among the different components of the genome: how many in protein coding genes, how many in introns, how many in pseudogenes, how many in SINEs and LINEs, and so on. 7) Now, we are really at a stop. because, to go on with our computations, and to verify how "amazing" is the coincidence which so much impresses Larry Moran (and, I suppose, you too), we should know: a) How big is X b) How the X mutations are distributed between the various components of the genome. 8) then we would have something. But still we should try to understand more about the function of non coding segments, and how robust they are to variation. Only if we take into account all these aspects, our reasoning becomes serious and quantitative. Then, maybe we can find really some "amazing coincidences". Maybe those coincidence would point strongly to a design explanation. I don't think I can be more clear and detailed than so.gpuccio
April 22, 2014
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Mung: I think we are saying the same thing, but I am arguing about the reasons why variation can be neutral. It's not enough to observe that variation is often neutral, we have also to understand why it is neutral. And I have tried to detial that the reasons for neutrality can be different. When a mutation appears in an active protein coding gene, it is neutral only if it does not affect the protein function, or at least not enough to be "seen" by negative selection. When a mutation happens in a non functional sequence, it is neutral by definition: there is no function to be affected, therefore all variation in that sequence will be neutral. When a mutation happens in a functional non coding gene, it will be neutral if it does not affect significantly the function of that non coding sequence, whatever it is. And the probability of a mutation in that sequence being neutral will be different from the probability of a mutation in a protein coding gene being neutral, because the function is different and is differently related to the sequence. Moreover, as non coding DNA has functions which can be very different, even different types of functional non coding DNA can have completely different tolerance to variation. I don't think these things are irrelevant. not at all. If we are discussing a theory about neutral variation, we must ask ourselves why variation is neutral in different contexts, especially if we are not just observing that some specific variation is neutral, but we are rather assuming that almost all the variation from one species to another is neutral, and from that assumption we are inferring that almost all the genome is non functional. I think that these considerations are very relevant. But if wd400 is not bothered by them, it's OK. :)gpuccio
April 22, 2014
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Good point.
I am not sure it is a good point. I can find no reference that repetitive sequences are not actually repetitive Saying they have rotted says they are not actually repetitive. They do not refer to them as formerly repetitive sequences. Or that the sequences can be seen to have been once repetitive. They are described as repetitive.
repetitive sequences are seen as evidence that supports the hypothesis of common descent of humans with other primate species, are they not?
Is this true? I assumed what is used for common descent is the conservation of coding regions, not the repetitive sequences. But I am certainly not sure of this and any references on this would be welcome. The term conserved means a lot of things. We all assume there is conservation within coding regions of a species. Isn't this what the discussion of the neutral theory is about, saying that it changes the coding regions in some places and this is the source of speciation. But for within the same species there is conservation of the coding regions. For similar species many of the coding regions across species are also conserved. This later fact is what is used to support common descent as you said. This also implies across long periods of time. Are non-coding regions such as repetitive regions also used to infer common descent? I am curious about this. The term conserved can also mean conserved sequences within the same species in non-coding regions amongst the various individuals of a species. For example within humans are there similar non coding sequences amongst individuals from various regions of the world. If so then this would indicate function for these regions. The study I pointed to indicated there was selection going on for many non-cocing regions. These regions were also repetitive. This is interesting because some are very vocal about repetition as an indication of junk. Then there is the other issue that I and Allen MacNeill bring up Namely, the variation that is created by Allen's list of engines of variation and how does this variation change over time. These are regions that really should rot or a better description is change randomly over time. This is claimed to be the source of new coding sequences for proteins or other functions as large parts of the genome which is truly junk mutates away.jerry
April 21, 2014
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Mung, Voles will/ should be the "poster child" for neutral theory. :cool:Joe
April 21, 2014
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gpuccio:
2) We cannot apply the same quantitative principles to mutations and neutrality in coding genes, functional non coding genes, and non functional non coding genes.
But if we are speaking of neutral theory, these are irrelevant, because neutral theory is not about those things and is not dependent upon those things. wd400:
Irrelevance piled upon irrelevance.
In one sense I clearly agree with you. Please comment on my post @ 96 and let me know if I am at least in the ballpark. Unless I am just mistaken, you're talking about neutral theory. gpuccio is attempting to place neutral theory in a wider context. In the context of neutral theory some of what he is writing is indeed irrelevant. But in the larger context, those things are relevant. So for the most part I think you two gentlemen are just talking past each other. But it's still entertaining! wd400, I certainly understand how this might be a "hostile" environment for you. You've no doubt been abused repeatedly for saying things that to you are just true on their face. But if you can find it within yourself, do what you can to make it clear when and where you and gpuccio are actually talking about the same thing and if not why not. I appeal to gpuccio to do the same. This is an interesting discussion! Let's find the ground that you both need to be on so that you are both discussing the same thing and not seeing what the other says as irrelevant. Am I correct in my theory that the disconnect is over what neutral theory is actually about?Mung
April 21, 2014
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gpuccio:
OK?
NOPE. You've turned neutral theory on its head! Neutral theory, similar to Punctuated Equilibrium, was devised to explain why certain observed facts did not align with Darwinian theory. It's not a theory about why this or that mutation is neutral and doesn't attempt to explain why this or that mutation is neutral. It's simply a statement that most "evolution" cannot be under selection! Along with some nice maths to support it. :) I'm sure we're saying the same thing, I just don't want people to be sidetracked on to what's a neutral mutation and lose sight of the bigger picture, that Darwinism is false. :DMung
April 21, 2014
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gpuccio:
On the other hand, your theory (neutral variation) is completely useless to explain what we observe (functional information in biological beings, and in particular the emergence of a lot of new functional information in a new species). So, it must recur to a completely different (and empirically unsupported) process, NS, to try to give some explanation. Therefore, your theory has no scientific credibility.
Walter ReMine calls evolutionary theory a smorgasbord. It's defenders pick and chose what they want or need at a particular moment in time to defend the particular argument they are making at the time. On the whole, "the theory" is incoherent. And yes, neutral theory does not and cannot explain "the appearance of design." It does not explain adaptation. Which is why Larry Moran is a hypocrite, because at heart, he is a Darwinian.Mung
April 21, 2014
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wd400:
Repetitive is a statement about sequence classes within a single genome... ...repetitive sequences do ‘rot’ over time, but just at the neutral rate which takes a while so we can still see the repeat motif.
Good point. But repetitive sequences are seen as evidence that supports the hypothesis of common descent of humans with other primate species, are they not? Now looking at JUST repetitive sequences in humans and other primate species, do they support the predictions of neutral theory? Do they exhibit the same or a different mutation rate?Mung
April 21, 2014
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What are your references for this? It seems that these sequences have been around for millions of years and with mutations in every genome in the population and recombination during reproduction, that any sequence would have been turned into a mush.
Mutations will just fix at the neutral rate - human and chimp genomes are 98.whatever percent similar after 6 million years of evolution and any two repeats will be as similar. In fact, for a given alu element there is a ~25% chance any two alus in the human and chimp genome will be indentical after 6 million years. The paper you linked to shows that ~18% of transcription start sites come from the ~50% of the human gnome that is made of repetitive elements, and ~10% of those transcription start sites produce an mRNA that is known (at the time, I guess there'd be more npw). Even if we made the mistake of thinking mRNA production = function we'd end up with repetitive elements have being less functional than the rest of the genome (which, I shouldn't need to stress, doesn't mean all such elements are function-less).wd400
April 21, 2014
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jerry: Thank you for the very interesting references. I don't think, however, that wd400 will be bothered by them. :)gpuccio
April 21, 2014
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repetitive sequences do ‘rot’ over time, but just at the neutral rate which takes a while so we can still see the repeat motif.
What are your references for this? It seems that these sequences have been around for millions of years and with mutations in every genome in the population and recombination during reproduction, that any sequence would have been turned into a mush. But yet the term repetitive is prevalent in all the literature. For example, Faulkner et al. The regulated retrotransposon transcriptome of mammalian cells Nature Genetics 41:5, 563-571 April 2009 http://subviral.med.uottawa.ca/~rna/ng.368.pdf
Although repetitive elements pervade mammalian genomes, their overall contribution to transcriptional activity is poorly defined. Here, as part of the FANTOM4 project, we report that 6–30% of cap-selected mouse and human RNA transcripts initiate within repetitive elements. Analysis of approximately 250,000 retrotransposon-derived transcription start sites shows that the associated transcripts are generally tissue specific, coincide with gene-dense regions and form pronounced clusters when aligned to full-length retrotransposon sequences. Retrotransposons located immediately 5' of protein-coding loci frequently function as alternative promoters and/or express noncoding RNAs. More than a quarter of RefSeqs possess a retrotransposon in their 3' UTR, with strong evidence for the reduced expression of these transcripts relative to retrotransposon-free transcripts. Finally, a genome-wide screen identifies 23,000 candidate regulatory regions derived from retrotransposons, in addition to more than 2,000 examples of bidirectional transcription. We conclude that retrotransposon transcription has a key influence upon the transcriptional output of the mammalian genome.
This study indicates a large number of non-coding regions are functional. Here they use the number 250,000. And apparently they are under positive selection pressures http://www.osc.riken.jp/english/activity/cage/achievements/ From this site:
These are under positive evolution, and our data show that the evolution of humans was caused not only by changes of protein sequences, but rather changes of RNA expression level driven by these CpG promoters, that are under positive selection in recent human lineages. CpG broad promoters are prevalent in brain, highlighting the complexity of transcriptional regulation in this tissue and the role of epigenetic control in the control of expression in the brain.
We should look into this phenomena more closely. Genomes from all over the world are now available and the number is increasing by large amounts each year. Apparently every research project using a new genome must submit their data for use by anyone else doing research. There are genomes dating back tens of thousands of years and there is a data set of the native populations of Australia, New Guinea and parts of the Philippines that separated from Africa about 70,000 years ago. So a lot of the ideas we speculate with could be answered by data available today or will shortly be available in the near future.jerry
April 21, 2014
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wd400: Well, you are entitled to your own opinions. I have tried to explain my point of view, and I don't think you have answered anything specific. You just stick yo your position. That's OK. I must remind you that neutral RV happens in functional sequences, even in protein coding genes, and at rates which cannot be anticipated with precision, especially when the function and its molecular basis are not known. I wonder if you will be bothered when biological research will confirm and enlarge the functions of non coding DNA, or if you will still stick to your beloved theory with its expectations. We don't see "most of the genome evolving at the neutral rate through time". 4% of non coding DNA is conserved, and part of it ultraconserved. Understanding of the remaining part is still very incomplete. You just see genomes evolving, maybe, at a rate which is not completely different from what you expect. Don't pretend that you have precise quantitative expectations, which are verified in detail. While neutral variation is certainly there, we have no evidence of how much of the variation is neutral, and how much is functional. Even you will admit that part of the variation must be functional, won't you? Otherwise, why are humans capable of doing things that chips cannot do? Or do you deny even that? Because, you know, that is the big question. How does functional novelty arise? How much neutral variation is there can be interesting, but in the end it is not really important. It's functional variation that we are interested in. You have said nothing about functional variation. Not where you think it takes place, not how much of it you think takes place, and especially nothing, nothing at all, about how it would take place, except for trying a tired and unconvinced revival of NS. Do you realize that functional variation is there, among the total variation? Do you realize that you should subtract it from the total variation, because it certainly is not neutral? Do you realize that what is neutral in a protein coding gene is different from what could be neutral in a regulatory gene, or in different types of regulatory genes? Do you realize that regulatory genes must be there? Have you subtracted a figure for them from your computations? Are you really being quantitative, or are you just trying to justify your theory with numbers ad hoc? The simple truth is that we should understand before how much of the genome is functional, and knowing that we could compute how much of variation is random, and how much of that random variation is neutral. Reasoning the other way round is pointless. You must ascertain function from functional studies, not from population genetics suppositions. That's the right way, the only way. That's what many biologists, including those at ENCODE and Mattick, whom you so much despise, are trying to do. But please, feel free not to be bothered by all those thing.gpuccio
April 21, 2014
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wd400:
Irrelevance piled upon irrelevance
That describes unguided evolution.
Scientists know a lot more about the regulation of gene expression than you do, but that doesn’t actually matter.
Knowing about something and being able to explain how unguided evolution produced it are two very different things. BTW design does NOT require outside force/intervention. And the branches on the evolutionary tree are imaginedJoe
April 21, 2014
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Irrelevance piled upon irrelevance. Scientists know a lot more about the regulation of gene expression than you do, but that doesn't actually matter. If most of the genome was functional then random variation (I remind you, your original claim, which you've apparently resiled from, was "Random Variation is mostly neutral") wpuld mostly be non-neutral unless biological functional is not sequence-specific. When we see most of the genome evolving at the neutral rate through time, and meeting the neutral expectation in populations we can conclude variation in most of the genome is of no consequence. It's very hard to imagine how that would be possible in a mostly functional genome. The counter, that variation is created by some outside force (?) at constant rate (how else would the branches on an evolutoinary tree relating Human, Neanderthal, Chimp, Gorilla have the same lengths) equal to the individual mutation rate is.... not really worth bothering with.wd400
April 21, 2014
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wd400 and all: I would like to discuss briefly a couple of concepts which, while implicit in much that I have said here, deserve probably better clarification. 1) Neutral random variation is of two different kinds. Variation can be neutral (in the sense that it does not influence existing function, and therefore is not subject to any process of selection, neither negative nor positive) for two different reasons: a) It happens in a functional region, but it does not affect its function. b) It happens in a non functional region. The first case is well known in protein coding genes. Many mutations can occur in a protein coding gene without affecting the protein function. There are different reaosn for that too: a1) The mutation is synonimous, and therefore it does not change the protein sequence (although it can sometimes affect its transcription and translation, but we will will not consider that aspect for the moment). That is a direct consequence of the redundancy of the genetic code. a2) The mutation does affect protein sequence, but the new sequence retains the same structure and function. That is the case when an AA is changed into a similar AA, and the structure is not significantly altered, or when other compensatory modifications happen at the same time in the sequence, or simply when the AA which changes is not part of a functionally important part of the protein. IOWs, that is a direct consequence of the redundancy of the protein functional space. There is also another consideration. A mutation can affect the function of a protein, but only in part, or the protein could just not be really relevant for survival and reproduction. In both cases, although the mutation is not really neutral, still it would escape the effects of selection. In the second case (b) the mutation is neutral by definition, because it happens in a non functional sequence. Not only a non coding sequence, but a non coding sequence which has no other function, be it regulatory or else. IOWs, a mutation occurring in a truly "junk" sequence. In this case, the mutation is neutral not because it does not affect significantly the function of the sequence, but because the sequence has no function in the beginning. OK? 2) We cannot apply the same quantitative principles to mutations and neutrality in coding genes, functional non coding genes, and non functional non coding genes. Let's start with non functional non coding genes, which are a part (we don't know how big) of the total non protein coding DNA (in humans, about 98% of the total genome). These sequences are non functional by our same definition, therefore any variation occurring in them is by definition neutral, and therefore neutral variation (of type b) will occur (and maybe fixed by drift) at the same rate as the general mutation rate. Unless they are designed variation, therefore building a new function. In that case, once the new function is complete and expressed (whatever it is) that variation will be subject to positive selection and fixation. In protein coding genes, the situation is different. Here, negative selection can fully act on variation, defending the existing function. IOWs, a relevant part of variation is no more neutral, and will be more or less efficiently eliminated by negative selection. IOWs, the sequence will show some (variable) degree of conservation. However, neutral mutations will still occur (of type a), and the sequence will change in time, to a certain degree, while retaining a minimum level of homology. The rate of variation, therefore, will be lower. It will vary from protein to protein, according to many variables, including the degree of functional information in the protein, as measure by the Durston method. But we can have a good idea of the mean rate of neutral variation in protein coding genes, because we know protein coding genes and proteins, we know the genetic code for protein synthesis, and we know much of the structure-function relationship in proteins. But what can we say of functional non coding DNA, IOWs, of non protein coding DNA with regulatory functions? First, we absolutely know that it exists, but we don't know how big a part of the total non coding DNA it is. Indeed, the ratio between functional non coding DNA and non functional non coding DNA is exactly what is at stake here, and is at present the object of a true was among biologists, as clearly seen in this same thread. Second, we know almost nothing of what it is, how it works, and what its structure-function relationship is. That's why we cannot absolutely apply to functional non coding DNA the same rules or expectations about variation neutrality that we apply to protein coding genes. Some things, however, we know: a) Whatever the regulatory function is, it is not based on the genetic code. IOWs, non coding functional genes are not written in codons intended to represent AAs. Therefore, the first cause of neutral variation in protein coding genes (synonimous mutations, due to the redundancy of the genetic code) does not apply here. b) We have no ideas about the functional redundancy of functional non coding sequences, because we know much less about them than about protein coding sequences. Indeed, in many cases we don't even know what the regulatory sequences are. So, we cannot even start to estimate how much a functional non coding sequence can change, while its function is retained. The chance for neutral variation can be higher than in protein coding genes, or lower. We have no idea. c) Another fundamental difference with protein coding DNA is that functional non coding DNA is certainly more heterogeneous. We know that non coding DNA is made of different types, very different one from the other: introns, satellites of various kinds, SINEs, LINEs, transposons, pseudogenes, and so on. For each of them, different rules can be valid about neutral mutation rate, because their functions will probably be different. We already know of different kinds of regulatory function, with different mechanisms, and the bulk is still to be discovered. Moreover, even the same type of non coding DNA (for example, introns) could have different mechanisms of function in different contexts. The final conclusion is that we have no way to compute how much variation we would expect to find in the sum total of the genome, if we consider all these different aspects.gpuccio
April 21, 2014
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Joe:
OK we get it. Blind and unguided processes cannot account for DNA but it can account for junk DNA.
Yes, you got it perfectly right! The simple point is that they are not interested in explaining functional information. They are only interested in self-justifying their artificial theories. "Who cares if humans have such a complex brain, and are the only biological beings which can develop abstract thinking and many other details? The important thing is that what is new in their genome could be the product of random neutral variation, if it were true that it is non functional. Well, that's an amazing scientific achievement, after all! :) And let's remind those IDiots, who still think that NS is the real (false) thing in biological naturalism, that we don't believe any more in the importance of NS. After all, neutral variation and drift can explain all our supposed junk. Ah, yes, if they just insist in asking how functional novelty arises, please remind them that NS can always easily explain all that. But beware, it is no more the important thing!"gpuccio
April 20, 2014
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