Richard Lenski's Long-Term Evolution Experiments with <i>E. coli</i> and the Origin of New Biological Information (Updated) - Evolution News & Views

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Richard Lenski's Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information (Updated)

e. coli bacteria

Intelligent Design and the Origin of Information: A Response to Dennis Venema

In this article, Part 5, we:
• Understand why Venema's citation of Lenski's "Long Term Evolution Experiments" do not demonstrate that "Complex, specified information can indeed arise through natural mechanisms"
• Review Michael Behe's 2010 paper in Quarterly Review of Biology which investigated Lenski's research and found that "mutations were decreasing or eliminating the protein's function"
• Investigate why Lenski's E. coli bacteria that evolved the ability to uptake citrate under oxic conditions didn't evolve anything new and likely experienced loss-of-molecular function

Other Installments:
Part 1: Intelligent Design and the Origin of Biological Information: A Response to Dennis Venema
Part 2: Why Did One Theistic Evolutionist Part Ways with BioLogos?
Part 3: What Is a Proper Test of Intelligent Design?
Part 4: The False Dichotomy Between Intelligent Design and Natural Causes
Part 6: Another Bogus Claim of "Novel Function Arising Through Mutation and Selection"
Part 7: Confusing Evidence for Common Ancestry with Evidence for Random Mutation and Natural Selection
Part 8: Critically Analyzing the Argument from Human / Chimpanzee Genetic Similarity

See below for the update.

Some critics of intelligent design (ID) misunderstand ID as a denial of natural causes. For example, we have recently seen how theistic evolutionist Dennis Venema wrongly suggests that, in both a scientific and theological sense, ID denies natural causes. Venema imports this misunderstanding into his proposed methods of testing ID, suggesting that if we find natural causes doing anything, then ID is refuted.

Venema writes: "any natural mechanism that can be shown to produce information would render [Stephen Meyer's] argument that information only arises from intelligent sources null and void."

Dennis Venema's argument collapses into this: 'if Darwinian evolution can do anything, then ID is wrong.' But this is not how we test ID, for ID readily allows that natural selection and random mutation can effect some changes in populations. The right question is not 'Can natural selection do anything?' but rather 'Can natural selection do everything?'

With this in mind, let's analyze Dr. Venema's discussion of Richard Lenski's Long Term Evolution Experiments ("LTEE") with E. coli.

Where's the Behe?

Before discussing the LTEE, it's important to note that from the beginning of his series for BioLogos on evolution and the origin of information, Venema didn't just purport to critique Stephen Meyer's arguments in Signature in the Cell. Rather he referred to rebutting the entire "Intelligent Design Movement" or what he called (following Judge Jones?) the "IDM."

But if Venema is going to critique the entire "IDM" using Richard Lenski's "Long Term Evolution Experiments," then Venema should discuss the most relevant literature of the "IDM" that discusses those experiments. He doesn't do that.

In Venema's discussion of the LTEE, there is no mention of a 2010 peer-reviewed scientific paper written by the most prominent biochemist in the "IDM," published in a prominent biology journal, extensively critiquing Lenski's LTEE. Venema fails to note and discuss Michael Behe's December 2010 paper in Quarterly Review of Biology (QRB), which extensively discusses and critiques Lenski's Long Term Evolution Experiments. Instead, Venema critiques the writings of Stephen Meyer, who hasn't commented on Lenski's LTEE because they weren't relevant to his arguments in Signature in the Cell about the origin of life.

By misrepresenting Meyer's thesis as being refuted by evidence of the power of natural selection, Venema creates a straw man. Meanwhile he ignores the substantive critiques by leading ID proponents of the very evidence he raises.

Vague Discussions vs. Precise Discussions of Lenski's LTEE

As an initial salvo regarding Lenski's LTEE, Venema writes:

[T]here were many possible genetic states of higher fitness available to the original strain, and random mutation and natural selection had explored several paths, all leading to a higher amount of "specified information" -- information that specifies increased reproduction and survival in the original environment. All this was by demonstrably natural mechanisms, with a complete history of the relevant mutations, the relative advantages they conferred, and the dynamics of how those variants spread through a population. The LTEE is at once a very simple experiment, and an incredibly detailed window into the inner workings of evolution.
But what exactly was the "specified information" that increased? What new function was gained? Where did natural selection and random mutation produce functional, information-rich genes and proteins? Venema doesn't say what new functions arose, what changed, or what information was gained. His claim that natural selection produced "specified information" is vague.

By contrast, in critiquing claims that the LTEE has produced something new, Behe's 2010 Quarterly Review of Biology paper was anything but vague:

By examining the DNA sequence of the E. coli in the neighborhood surrounding the IS [insertion sequence] elements, the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others. In subsequent work, Cooper et al. (2001) discovered that twelve of twelve cell lines showed adaptive IS-mediated deletions of their rbs operon, which is involved in making the sugar ribose. Thus, the adaptive mutations that were initially tracked down all involved loss-of-FCT.

Several years later, when the cultures had surpassed their 20,000th generation, Lenski's group at Michigan State brought more advanced techniques to bear on the problem of identifying the molecular changes underlying the adaptation of the E. coli cultures. Using DNA expression profiles, they were able to reliably track down changes in the expression of 1300 genes of the bacterium, and determined that 59 genes had changed their expression levels from the ancestor, 47 of which were expressed at lower levels (Cooper et al. 2003). The authors stated that "The expression levels of many of these 59 genes are known to be regulated by specific effectors including guanosine tetraphosphate (ppGpp) and cAMP-cAMP receptor protein (CRP)" (Cooper et al. 2003:1074). They also noted that the cellular concentration of ppGpp is controlled by several genes including spoT. After sequencing, they discovered a nonsynonymous point mutation in the spoT gene. When the researchers examined ten other populations that had evolved under the same conditions for 20,000 generations, they found that seven others also had fixed nonsynonymous point mutations in spoT, but with different substitutions than the first one that had been identified, thus suggesting that the mutations were decreasing the protein's activity.

The group then decided to concentrate on candidate genes suggested by the physiological adaptations that the cells had made over 20,000 generations. One such adaptation was a change in supercoiling density; therefore, genes affecting DNA topology were investigated (Crozat et al. 2005). Two of these genes, topA and fis, had sustained point mutations. In the case of topA, the mutation coded an amino acid substitution, whereas, with fis, a transversion had occurred at the fourth nucleotide before the starting ATG codon. The topA mutation decreased the activity of the enzyme, while the fis mutation decreased the amount of fis gene product produced.

(Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

If you weren't following all the technical language, here's what's going on: For the first 20,000 generations of Lenski's LTEE, very little happened. There were a few molecular adaptations observed, yet whenever we understood their molecular basis, they involved the knocking out of genes, or decreasing protein activity -- in essence, a decrease in specificity. Behe summarizes:
The fact that multiple point mutations in each gene could serve an adaptive role -- and that disruption by IS insertion was beneficial -- suggests that the point mutations were decreasing or eliminating the protein's function.

(Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010) (emphasis added).)

Unlike Venema's discussion, Behe's is precise, giving multiple examples and detailed descriptions of the types of changes observed in Lenski's LTEE. And Behe found that the types of changes taking place in the E. coli tended to decrease or eliminate protein function.

Before getting into a discussion of the citrate-using strain of E. coli, Behe closes with another specific example that involved decreasing gene activity in Lenski's LTEE:

In an investigation of global protein profiles of the evolved E. coli, Lenski's group discovered that the MalT protein of the maltose operon had suffered mutations in 8 out of 12 strains (Pelosi et al. 2006). Several mutations were small deletions while others were point mutations, thus suggesting that decreasing the activity of the MalT protein was adaptive in minimal glucose media.
Looking at Table 3 of Behe's QRB paper, not a single example of an adaptive mutation in Lenski's LTEE entailed a gain of a new molecular function. In fact, over the course of his entire paper, Behe goes further and explains that most of our known examples of molecular adaptations in bacteria entail "loss-of-function" mutations. Somehow, Venema doesn't discuss any of these findings.

E coli. Could Uptake and Metabolize Citrate Before Lenski's LTEE

Later, when referring to a different stage of the LTEE, Venema claims that a new function did arise in Lenski's E. coli bacteria during the experiments: the ability of E. coli to metabolize citrate. Venema claims that "One of the defining features of E. Coli is that it is unable to use citrate as a food source," but after a series of mutations "bacteria that use citrate dominate the population." According to Venema, these experiments show "Complex, specified information can indeed arise through natural mechanisms."

Yet Venema leaves out important details, creating an inaccurate impression. As we'll discuss below, normal E. coli already have machinery to uptake and metabolize citrate, so the general fact that Lenski's bacteria showed this ability is really quite unremarkable.

Unfortunately, Venema's readers on the BioLogos will never hear that. They also won't learn that Michael Behe has written extensively about Lenski's research, showing that the machinery for E. coli to uptake and metabolize citrate already existed in these bacteria. This isn't an entirely new biochemical pathway. Venema fails to note that normal E. coli already have the ability to uptake and metabolize citrate. They just can't normally uptake it under oxic conditions; Lenski's bacteria evolved the ability to uptake it under oxic conditions used in the experiment. Then the E. coli used their normal metabolic pathways to use citrate as a food source. Behe made this point while commenting on these claims soon after they were first published in 2008:

Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it's not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a "citrate permease" which can transport citrate from outside the cell through the cell's membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, "The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions." (1)

(Michael Behe, Amazon Blog, "Multiple Mutations Needed for E. Coli" (June 6, 2008).)

Likewise, Behe's recent 2010 paper in Quarterly Review of Biology provided an extensive critique of claims that Lenski's LTEE showed the evolution of a new pathway that could metabolize citrate. Venema doesn't cite or mention Behe's QRB paper, but it too explains that E. coli already had the ability to metabolize citrate. Behe explains:
Recently, Lenski's group reported the isolation of a mutant E. coli that had evolved a Cit+ phenotype. That is, the strain could grow under aerobic conditions in a culture of citrate (Blount et al. 2008). Wild E. coli cannot grow under such conditions, as it lacks a citrate permease to import the metabolite under oxic conditions. (It should be noted that, once inside the cell, however, E. coli has the enzymatic capacity to metabolize citrate.) The phenotype, whose underlying molecular changes have not yet been reported, conferred an enormous growth advantage because the culture media contained excess citrate but only limited glucose, which the ancestral bacteria metabolized.

(Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

Thus, Behe explains that the precise genetic mechanisms that allowed E. coli to uptake citrate under oxic conditions are not known. But Behe goes further and points out that the citrate-metabolizing E. coli strains really aren't anything new, and that previous investigations suggest that the ability of the E. coli to uptake citrate under oxic conditions might result from molecular loss-of-function:
As Blount et al. (2008) discussed, several other laboratories had, in the past, also identified mutant E. coli strains with such a phenotype. In one such case, the underlying mutation was not identified (Hall 1982); however, in another case, high-level constitutive expression on a multicopy plasmid of a citrate transporter gene, citT, which normally transports citrate in the absence of oxygen, was responsible for eliciting the phenotype (Pos et al. 1998). If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.


(Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

Thus, previous research suggests that the adaptation which allowed these E. coli to uptake citrate under oxic conditions might be caused "by the loss of the activity of a normal genetic regulatory element." Here's what is likely going on here:
  • Under normal conditions, E. coli can metabolize citrate; after all metabolizing citrate is an important step in the Krebs cycle, a pathway used by virtually all living organisms when creating energy.
  • But under oxic conditions, E. coli lack the ability to transport citrate through the cell membrane into the cell. E. coli can do this under reducing conditions, but under oxic conditions E. coli can't normally uptake citrate.
  • If Lenski's citrate-using E. coli are like previous E. coli which were discovered uptaking citrate under oxic conditions, then it seems likely that the bacteria underwent a mutation that knocked out the regulation mechanism of a citrate-transport gene, causing over-expression, allowing the E. coli to uptake citrate under oxic conditions.
In other words, the machinery for both transporting and metabolizing citrate was already present in these bacteria. But a series of knockout mutations broke the regulation of pre-existing citrate transport mechanisms, causing over-expression of a citrate transport gene, allowing citrate to be transported under both oxic and anaerobic conditions. If this is the case, then clearly this example of Darwinian "evolution" entails the loss of a molecular function, not the gain of a new one. And there was no wholesale acquisition of the ability to metabolize or, as Venema put it, "use" citrate.

In fact, as Behe notes, we don't really yet understand the precise molecular mechanisms that caused these E. coli to be able to uptake citrate under oxic conditions. So as far as we can tell, these changes entailed the origin of no new functional genes or proteins but might have resulted from a broken regulatory mechanism. We have not seen that natural selection and random mutation can produce functional, information-rich genes and proteins, and Venema is wrong to suggest otherwise.

Contra Venema, this example hardly shows the Darwinian evolution of a "new function," especially since E. coli already had the ability to uptake and metabolize citrate. Venema claims that CSI has arisen, but if we don't even know what mechanisms were involved in this change, how does he know that it is new CSI?

What do Lenski's LTEE Really Tell Us?

In his QRB paper, Behe goes on to explain that to date, the known adaptations that have occurred in Lenski's LTEE are either modification-of-function or loss-of-function changes:

The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski's research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.

(Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

Behe's paper further suggests that when there are several kinds of potential adaptive mutations that might occur, loss or modification of function adaptations will be far more common than gain-of-function adaptations. He concludes:
Even if there were several possible pathways by which to construct a gain-of-FCT mutation, or several possible kinds of adaptive gain-of-FCT features, the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.

(Michael J. Behe, "Experimental Evolution, Loss-of-Function Mutations and 'The First Rule of Adaptive Evolution'," Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

The sort of loss-of-function examples seen in the LTEE will never show that natural selection can increase high CSI. To understand why, imagine the following hypothetical situation.

Consider an imaginary order of insects, the Evolutionoptera. Let's say there are 1 million species of Evolutionoptera, but ecologists find that the extinction rate among Evolutionoptera is 1000 species per millennium. The speciation rate (the rate at which new species arise) during the same period is 1 new species per 1000 years. At these rates, every thousand years 1000 species of Evolutionoptera will die off, while one new species will develop--a net loss of 999 species. If these processes continue, in 1,000,001 years there will be no species of Evolutionoptera left on earth.

If Behe is correct, then Darwinian evolution at the molecular level faces a similar problem. If, all other things being equal, a loss or modification of function adaptation is generally 100-1000 times more likely than gain of function adaptations, then eventually an evolving population might run out of molecular functions to lose or modify. Neo-Darwinian evolution cannot forever rely on examples of loss or modification-of-function mutations to explain molecular evolution. At some point, there must be a gain of function.

Vaguely Appealing to Vast Probablistic Resources Won't Work

Venema closes his post on the LTEE by saying: "what the IDM claims is impossible, these 'tiny and lowly' organisms have simply been doing -- and it only took 15 years in a single lab in Michigan. Imagine what could happen over 3,500,000,000 years over millions of square miles of the earth's surface."

But vague appeals to vast eons of time and huge population sizes are unconvincing. You just have to do the math. As David Abel reminds us:

Mere possibility is not an adequate basis for asserting scientific plausibility. A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, "Yes." ... One chance in 10200 is theoretically possible, but given maximum cosmic probabilistic resources, such a possibility is hardly plausible. With funding resources rapidly drying up, science needs a foundational principle by which to falsify a myriad of theoretical possibilities that are not worthy of serious scientific consideration and modeling.

(David L. Abel, "The Universal Plausibility Metric (UPM) & Principle (UPP)," Theoretical Biology and Medical Modelling, Vol. 6:27 (Dec. 3, 2009).)

In the case of E. coli and citrate, the bacteria already had the ability to uptake and metabolize citrate, and simply found a way to transport it under different conditions. It's likely this occurred by overexpressing pre-existing transport mechanisms. Does this imply that anything and everything "could happen over 3,500,000,000 years over millions of square miles of the earth's surface"? Well, ID proponents aren't interested in making vague and ambiguous appeals to vast amounts of probabilistic resources. They want to test these questions, and follow the evidence where it leads.

As discussed here, ID proponents have asked just how long it takes to evolve traits that require multi-mutation features. A multi-mutation feature requires multiple mutations to be present before there is any advantage given to the organism. Doug Axe's research makes assumptions very generously favoring Darwinian evolution. He assumed the existence of a huge population of asexually reproducing bacteria that could replicate quickly -- perhaps nearly 3 times per day -- over the course of billions of years. Yet even here, complex adaptations requiring up to six mutations with neutral intermediates can become fixed. Beyond that, things become implausible.

If only slightly maladaptive intermediate mutations are required for a complex adaptation, only a couple (at most two) mutations could be fixed. If highly maladaptive mutations are required, the trait will never appear. Axe discusses the implications of his work:

[T]he most significant implication comes not from how the two cases contrast but rather how they cohere -- both showing severe limitations to complex adaptation. To appreciate this, consider the tremendous number of cells needed to achieve adaptations of such limited complexity. As a basis for calculation, we have assumed a bacterial population that maintained an effective size of 109 individuals through 103 generations each year for billions of years. This amounts to well over a billion trillion opportunities (in the form of individuals whose lines were not destined to expire imminently) for evolutionary experimentation. Yet what these enormous resources are expected to have accomplished, in terms of combined base changes, can be counted on the fingers.

(Douglas D. Axe, "The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations," BIO-Complexity, Vol. 2010(4):1-10.)

If Axe is correct then we cannot always assume, as Venema seems to do, that sufficient probabilistic resources exist to produce complex features we see in life.

Summarizing Venema's Argument Regarding the LTEE

In short, Venema's argument regarding the LTEE collapses into common misconceptions about ID, which go something like this:

  • (1) ID holds that Darwinian evolution cannot do anything.
  • (2) If Darwinian evolution can do something then it can do anything.
  • (3) Lenski's experiments show Darwinian evolution can allow E. coli bacteria to evolve a "new function" of metabolizing citrate.
  • (4) Therefore ID is wrong, and given enough time, Darwinian evolution can do anything we "imagine."
At each step in his argument, the facts and/or the logic is wrong:
  • Regarding (1): In fact, ID does not hold that Darwinian evolution can't do anything. Rather it claims that natural selection can do some things, but not everything. ID proponents readily acknowledge (as Behe has) that "if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it." The problem comes when multiple mutations are required to produce some new structure -- and as Axe's research shows, this is where Darwinian evolution typically gets stuck.
  • Regarding (2): Darwin-defenders have a long history of over-extrapolating from the data. ID is scientifically cautious and concludes that no one single experiment can show that Darwinian evolution can do everything we ask of it. A single experiment showing the ability of Darwinian evolution to do X simply shows the ability of Darwinian evolution to do X; it doesn't necessarily show Darwinian evolution can do Y, Z, and A, B, and C, etc. ID says we need to test hypotheses carefully and not over-extrapolate from observed data.
  • Regarding (3): In fact Lenski's experiments did not show the Darwinian evolution of an entirely new function. E. coli bacteria already had the ability to uptake and metabolize citrate, and the experiments simply showed they evolved the ability to uptake it under oxic conditions. This very likely required the loss of a molecular function.
  • Regarding (4) ID proponents do not think it is wise or scientifically accurate to vaguely invoke vast eons of time or vast population sizes to document the alleged power of Darwinian evolution. ID cautions that Darwinian evolutionists often assume that there are sufficiently vast probabilistic resources to accomplish any task imaginable, but that assumption might not be valid. Rather than simply assuming, Doug Axe's research finds that adaptations requiring more than six neutral mutations, or two maladaptive mutations, to provide a functional advantage would not arise in the history of the earth.
Subsequent research by Axe and Ann Gauger suggests that it would not be uncommon for Darwinian evolution to face obstacles that exhaust the probabilistic boundaries as found by Axe's research. In 2011, they published research in BIO-Complexity that found at least seven mutations (probably many more) would be necessary to convert one protein into a supposedly closely-related protein.

While Darwinians may (or may not) claim that this was a real evolutionary pathway, it's the type of pathway that is often claimed to have been traversed by natural selection over the course of life's history. The fact that this simple conversion required more mutations to produce a new function than would be allowed under Axe's mathematical models shows that there may be real obstacles to the Darwinian evolution of new proteins. Venema's citation of Lenski's LTEE certainly does not show otherwise.[Update, 9/25/2012: About a year after this article was first posted, Richard Lenski's lab has now published a paper which tries to elucidate some of the biochemical changes that allowed E. coli to metabolize citrate under oxic conditions in the lab. Ann Gauger has an excellent analysis of this paper at "Innovation or Renovation?," where she observes:

In his paper in Quarterly Review of Biology, Dr. Michael Behe pointed out that E. coli was already capable of using citrate for anaerobic growth (when no oxygen was available). He postulated that a change in gene regulation could turn on citrate transport and permit growth on citrate under aerobic conditions.

After an enormous amount of work, having sequenced the genomes of many clones along the lineages that led to the ability to use citrate, as well as lineages that never did, and testing the phenotypes of identified mutations, Blount et al. have now reported that Behe was largely right. The key innovation was a shift in regulation of the citrate operon, caused by a rearrangement that brought it close to a new promoter.
Gauger concludes: "But does this adaptation constitute a genuine innovation? That depends on the definition of innovation you use. It certainly is an example of reusing existing information in a new context, thus producing a new niche for E coli in lab cultures. But if the definition of innovation is something genuinely new, such as a new transport molecule or a new enzyme, then no, this adaptation falls short as an innovation. And no one should be surprised."]


33 Comments

Hi Nick,

Thanks for taking the time to write a reply. Sorry it took me a few days to find time to reply.

I’d like to begin this reply by talking a little bit about framing. You framed your response as pointing out a bunch of things that I supposedly "missed". That would imply that you raised something, expecting me to reply, but then I didn't.

Having looked back over your prior comment, I can't see how I "missed" responding to anything. I’ll talk about this a little in my reply.

But that’s not my main point.

In your original comment you framed my criticisms of neo-Darwinian evolution as if my “only response” is to call Darwinian mechanisms “magic.” This was unfair and inaccurate and it mischaracterized my arguments.

In my prior comment, I thoroughly rebutted your mischaracterizations of my arguments. Now, you have not replied. So rather than me having “missed” something, you have failed to justify you claim that my “only response” is to call Darwinian arguments “magic.” We’ll talk more about framing and misrepresenting arguments as this comment progresses.

Nick wrote: "Agree or disagree -- Michael Behe accepts that evolution can produce new genes, and thus new information."

I reply: I wasn't aware I had "missed" anything here because I was not aware I was supposed to reply to your prior assertions about Behe's views. I'm not sure why Behe's views are so important to you, but here's how I would describe them:

As we all know, Michael Behe believes there is an ‘edge’ to evolution, and thus he doesn’t believe that random mutation + natural selection (RM + NS) can do everything. So if you’re hoping Behe might say that RM + NS can do anything, you’re going to be sorely disappointed. Wherever Behe and Meyer might sit in the spectrum of what unguided natural evolutionary causes can or cannot do, they’re pretty close to one-other, and pretty far from typical neo-Darwinism.

Based upon Behe’s arguments in Darwin’s Black Box, The Edge of Evolution, his 2004 paper in Protein Science, and other sources, it’s pretty clear that Behe believes that features which require multiple simultaneous coordinated mutations to produce an advantage are unlikely to produced by random mutation and natural selection. Now, if a new gene can be produced in a stepwise fashion where each stepwise mutation yields an advantage, then I’m sure he’d say there's a chance there will be sufficient probablistic resources for Darwinian evolution to do the job. But if two or more mutations are required to get an advantage, the likelihood decreases dramatically (especially in multicellular organisms), and Behe would become skeptical of Darwinian mechanisms.

Rather than agreeing to some blanket statement that ‘evolution can produce new genes, and thus new information’, I think Behe would make a much more principled argument—perhaps something like this: ‘if one point mutation is required to gain an advantage, that could happen; if two or more are required, Darwinian evolution might be in trouble.’ That’s how I’ve seen Behe describe his views in my experience. In fact, he said something very much like this when commenting on Lenski's research:

“if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it. But if more than one is needed, the probability of getting all the right ones grows exponentially worse.”

For the record, I would agree with Behe's statement.

Nick wrote: "Please define 'fundamentally new'"

I reply: Again, I wasn't aware that I "missed" anything here because you hadn't asked me previously to define this. In any case, if you look at what I wrote, I was trying to describe Meyer's position, and the phrase "fundamentally new" belongs to Steve Meyer.

Behe, now Meyer...you keep asking me to define other people's positions, and I really don't want to put words into other people's mouths via speculation. If I'm going to describe someone else's positions, I prefer to quote from their works directly.

My point in quoting Meyer was to say the following: "the examples Venema offers did not demonstrate new genetic information arising in the form of, as Meyer asks for it, 'fundamentally new genes and proteins.'"

How do I know this is the case? This article is about Lenski’s LTEE research, and as we've seen, it has not been demonstrated that Lenski's E. coli bacteria have evolved any new genes or proteins. They don't even know what molecular mechanisms allow the mutant E. coli strain to uptake citrate under oxic conditions. From past experience, we know this phenotype could arise simply by breaking a gene regulation mechanism so it no longer functions. So whatever Meyer meant precisely by "fundamentally new genes and proteins", it's pretty clear that Lenski's experiments didn't produce it, because it hasn't been demonstrated that there are even any new genes or proteins in Lenski's bacteria. Once investigators identify the genetic and molecular mechanisms allowing Lenski's bacteria to uptake citrate under oxic conditions, we can debate whether they entail genes or proteins that are "fundamentally new." Until then, Venema (and others) should not claim that we know this experiment shows the evolution of “fundamentally new genes and proteins.”

Unfortunately Venema's inaccurate discussions of this experiment seem to be misleading people about what we know about Lenski's experiments. For example, a couple months after Venema's original post, some theistic evolutionist claimed here that Lenski's experiment showed "entirely new biological pathways". The purpose of my article here is to show that we definitely don't know that this is the case.

My purpose in this series is to respond to Venema's arguments. In that regard, my argument has two-steps:

(1) In a prior article, I pointed out that Meyer's thesis in Signature in the Cell doesn't pertain to biological evolution and the diversification of life, but rather to chemical evolution and the origin of life. So attempts to demonstrate that natural selection and random mutation can produce new biological information cannot respond to Meyer's argument, because natural selection and random mutation could not operate prior to the origin of replication.

(2) If we charitably ignore the severe deficiency in Venema's argument pointed out in step-one, and look at Venema's examples of natural selection and random mutation in action, he still hasn't shown that they have produced, as Meyer puts it, "fundamentally new genes and proteins". This article is part of my attempt to show that.

So what exactly does Meyer mean by "fundamentally new genes and proteins"? I'm not going to try to speculate about exactly what Meyer means by that, because, again I'm not inside his head. Again, we're talking about a brief statement from Meyer in an appendix, dealing with a subject that is not the main topic of his book, so it’s not surprising that it wasn't his book's purpose to flesh out in detail what he means by that. Maybe in the future he will.

But I can tell you what Meyer has said before, and it is very similar to Behe. As I said, wherever Behe and Meyer might sit in the spectrum of what unguided natural evolutionary causes can or cannot do, they’re pretty close to one-other, and pretty far from typical neo-Darwinism. In the same appendix you've been quoting from, Meyer makes an argument that is similar to Behe, and it gives us a very good idea of at least part of what he means by "fundamentally new":

[F]or mutation and selection to produce new functional proteins or protein folds--the smallest unit of selectable function--new proteins or protein folds must first arise by chance--that is, by random mutation. If the probability of this is extremely low--beyond the reach of available probablistic resources--then this would undermine the plausibility of the neo-Darwinian mechanism ... Thus, as a specific test of the efficacy f the neo-Darwinian mechanism (as well as the chance origin of information in a prebiotic setting), Axe posed the question: How rare or common are functional protein folds within their corresponding amino acid-sequence space? He realized that if functional sequences were common enough for mutations to stumble upon them relatively easily (within the time required for relevant evolutionary transitions), mutation and selection might be able to build otherwise extremely improbable structures in small incremental steps. On the other hand, if functional proteins are extremely rare within sequence space, such that mutations will not have a realistic chance of finding them in the available time, selection will have little or nothing to work on, undermining its ability to produce biological information. (Signature, pp. 494-495)

Nick wrote: "Creationists/IDists regularly use such vague language as an escape hatch when their claims are under pressure, but they never give a precise, scientific definition of 'fundamentally new'."

I reply: In the quote above, we saw that Meyer gave us a precise, scientific definition of at least part of what is entailed in a "fundamentally new protein": a protein with an entirely new fold. And he goes further in explaining why neo-Darwinism struggles to produce "fundamentally new" proteins: functional protein folds appear to be isolated in sequence space and it would thus be extremely improbable to transition through sequence-space from one fold to the next in small, incremental steps. Many mutations would be necessary before a new functional fold could arise, which is exactly why it is not going to discoverable by a blind trial-and-error process like random mutation and natural selection. Meyer's explanation of why fundamentally new proteins cannot be built by random mutation and natural selection is both principled and precise. By your terms Nick, I guess that means he's not under pressure and not a creationist, right?

I'm aware of your strategy to attempt to conquer ID by dividing ID proponents. But now, we see that in terms of substance, Meyer's position is pretty much identical to Behe's:

Both agree that natural selection works well when it can build "structures in small incremental steps" (Meyer) since "if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it" (Behe). But they also agree that when structures "are extremely rare within sequence space" then "mutations will not have a realistic chance of finding them in the available time" (Meyer), because "if more than one is needed, the probability of getting all the right ones grows exponentially worse" (Behe). In this regard, Behe's and Meyer's positions about what Darwinian mechanisms can or cannot do seem pretty much identical.

Nick wrote: "Please note that if 'fundamentally new' means 'no significant sequence similarity to other genes, then, at the very least, most of most genomes is not 'fundamentally new' and thus could have evolved from common ancestors without violating Meyer's 'law'."

I reply: I can see why you're confused here Nick. You mistakenly think that sequence similarity is evidence of a Darwinian pathway. It isn't. At most, it's just evidence of common descent. Behe points this out when he says:

"Although useful for determining lines of descent ... comparing sequences cannot show how a complex biochemical system achieved its function—the question that most concerns us in this book. By way of analogy, the instruction manuals for two different models of computer put out by the same company might have many identical words, sentences, and even paragraphs, suggesting a common ancestry (perhaps the same author wrote both manuals), but comparing the sequences of letters in the instruction manuals will never tell us if a computer can be produced step-by-step starting from a typewriter. ... Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form?" (Darwin's Black Box, pp. 175-176.)

"[M]odern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation." (The Edge of Evolution, p. 95.)

The fact that two sequences are similar doesn't necessarily imply that there is a functional stepwise Darwinian pathway from one sequence to the other. So when ID proponents challenge natural selection and random mutation, they want to know if there is a stepwise pathway from one sequence to the next.

Axe's recent paper with Ann Gauger showed why this is the case. They studied two proteins, Kbl and BioF, with different functions but highly levels of homology—and are thus thought by evolutionists to be very closely related. Through mutational analysis, Gauger and Axe found that a minimum of seven independent mutations—and probably many more—would be necessary to convert Kbl into the function of its allegedly close genetic relative, BioF. Per Axe’s December 2010 BIO-Complexity paper, they report that this is beyond the edge of evolution:

The extent to which Darwinian evolution can explain enzymatic innovation seems, on careful inspection, to be very limited. Large-scale innovations that result in new protein folds appear to be well outside its range. This paper argues that at least some small-scale innovations may also be beyond its reach. If studies of this kind continue to imply that this is typical rather than exceptional, then answers to the most interesting origins questions will probably remain elusive until the full range of explanatory alternatives is considered.

(Ann K. Gauger and Douglas D. Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway,” BIO-Complexity, Vol. 2011(1) (2011).)

(Please note: I'm well-aware of the standard rejoinder to this paper that this is not an actual evolutionary pathway that is claimed to have historically occurred. Axe and Gauger are well-aware of that fact and this doesn't rebut their argument. The problem is this: even if it wasn't a historical pathway, it's precisely the kind of pathway which evolutionists regularly claim can be easily traversed by natural selection and random mutation. Yet even this purportedly 'simple' transition between two closely related proteins appears to be beyond the edge of evolution.)

The point is this: the fact that two proteins share sequence similarity doesn't necessarily mean there is a stepwise Darwinian pathway between the two sequences. Perhaps it works like this: Two sequences that are very distant in sequence space and share no homology almost assuredly are not connected by a stepwise Darwinian pathway, but we're now finding (to the surprise of many Darwinians) that even proteins with similar sequences might not be amenable to stepwise Darwinian evolution.

Nick wrote: "So, if mutation and natural selection produce 10 bits, what magical process stops them from adding another 10 bits, and another 10 bits after that?"

I reply: This comment on your part reflects a fundamental misunderstanding of ID arguments. As we've discussed, Darwinian evolution can work when one mutation can provide some functional advantage to an organism. But when multiple mutations are necessary before there is any benefit, then intermediate mutational steps provide no benefit. Jerry Coyne explains why this is a problem for Darwinian evolution:

“It is indeed true that natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism.”

(Jerry Coyne, "The Great Mutator," The New Republic (June 14, 2007).)

Now Coyne claims he knows of no example where this is the case, but ID proponents have uncovered many such examples. Let's apply this problem to your hypothetical:

In DNA, each base pair represents more or less 2 bits of information. Roughly speaking, adding 10 bits of information might entail 5 mutations. If each successive mutation provides a stepwise selective advantage, then Darwinian evolution will probably be able to traverse the pathway of 5 mutations. As we saw above, both Behe and Meyer acknowledge this.

But let's say that there's no selective advantage until all 5 mutations are in place. In that case, even getting 10 bits of information by Darwinian evolution is going to be a lot harder. Doug Axe's December 2010 paper in BIO-Complexity shows this is beginning to push the limit of what is possible in the history of the earth:

Comments cannot display images so please click here for diagram

In the figure linked above, the x axis represents the number of mutations necessary for the trait to arise and confer some benefit to the organism. The y axis represents the base-10 logarithm of the number of generations required to fix the trait. Thus, if you're at the coordinate x=5, y=8, then it would take the 10^8 generations to fix a trait that requires 5 mutations before conferring any advantage. At point x = 5, y = 20, it would take 10^20 generations to fix a trait that requires 5 mutations to provide a benefit. In this diagram, anything that requires a total number of generations above the dashed lines would exhaust the maximum number of probabilistic resources available for an evolving population of bacteria over the entire age of the earth. (Since Axe modeled asexually reproducing bacteria, obviously far fewer probabilistic resources would be available for multicellular organisms—especially sexually reproducing ones—meaning fewer mutations would be possible.)

According to the graph, 5 neutral mutations would take 100,000,000 generations, or 100,000 years. So this is probably do-able (so long as we’re talking about rapidly reproducing microorganisms like bacteria and not multicellular organisms).

But if some (or all) of those 5 mutations are slightly deleterious then very quickly you could exceed the maximum probabilistic resources available in the history of the earth. For example, if just 3 of those mutations are only slightly deleterious (s = -0.0001), then you’ll quickly find yourself at the point x=3, y=12, which exceeds the maximum probabilistic resources available in the history of the earth. So it’s entirely possible that in many circumstances, adding just 10 bits of information to the genome is beyond the maximum probabilistic resources available in the history of the earth.

But let’s now add a new twist to our hypothetical. Let’s say that on our way to adding 500 bits of information, we encounter one intermediate stage where 7 neutral mutations are required to get any selective advantage. Again, looking at the diagram above, we see this step alone would exceed the maximum probabilistic resources available over the history of the earth, even if the mutations are merely neutral, and not at all deleterious.

And again, these numbers apply to rapidly reproducing microorganisms like bacteria, which likely give Darwinian evolution its best shot. If we’re talking about multicellular organisms – especially sexually reproducing ones – where generations don’t tick by nearly so quickly, then the probabilistic resources available to Darwinian processes are severely diminished, and even fewer mutations could arise for such features where no advantage arises until multiple mutations are present.

So it’s not at all clear that in all cases we could add 500 bits of information to the genome in a stepwise fashion. Darwinian theory only works if the steps stay below the dotted line. How do you know that all intermediate steps, and all traits, can evolve in a sufficiently stepwise manner so as to stay below that level?

Nick wrote: “Also, what prevents the process happening serially? Even if you accept that each case of a successful gene duplication+mutation+selection event produced only 1 bit of new information beyond what existed in the ancestral genes, then all that has to be done is find 500+1 such cases and Meyer's law is falsified.”

I reply: “Gene duplication+mutation+selection” can only occur in a biological context. As I noted in my prior comment, Meyer’s law applies only in a nonbiological context:

Here’s my version of the law of conservation of information: “In a nonbiological context, the amount of specified information initially present in a system, S, will generally equal or exceed the specified information content of the final system, Sf.” (Signature, p. 293)

So once again, you are explicitly ignoring Meyer’s law. Why do you insist on claiming Meyer’s law is falsified by evidence which explicitly is outside the context of his argument?

There’s no question that the ability of gene duplication+mutation+selection to produce new information is of interest to the scientific debate over intelligent design and neo-Darwinian evolution. However, Meyer’s argument applies only to the origin of life, and the causes which could have applied in that setting.

Natural selection requires replication. Prior to the origin of life, there was no replication. So how is “gene duplication+mutation+selection” going to produce new information prior to the origin of replication?

Your hypothetical does not touch upon Meyer’s law.

(And where did those “ancestral genes” come from? Are you sure that they could arise by random mutation and natural selection? That seems like another assumption you are making.)

Nick wrote: “Do you really think that fewer than 500 such cases have appeared, ever, in the whole history of life?”

I reply: Again, why did you insist on repeatedly misrepresenting Meyer’s argument, which doesn’t apply to the “whole history of life” but simply only applies to the origin of life?

And since you’re framing the issue in terms of “Do you really think,” since you deny intelligent design, do you really think that every trait which exists can evolve in a stepwise fashion?

Nick wrote: “[I]f you're going to rule out the biological case of the increase of information, because natural selection didn't exist at the origin of life and thus can't explain it, then you can just as well rule out intelligence as a cause of the origin of life, because it didn't exist then either, as far as we know. Fair is fair.”

I reply: It’s pretty simple why your argument is wrong: We have principled reasons for understanding why natural selection could not operate prior to the origin of life: natural selection requires replication, and prior to the origin of life, there was no replication.

Don’t take my word for this. Meyer quotes various authorities (including Nobel Laureate Christian de Duve making the same point):

[M]any scientists recognized that Oparin's concept of prebiotic natural selection begged the question. Natural selection occurs only in organisms capable of reproducing or replicating themselves. Yet, in all extant cells, self-replication depends on functional and, therefore, sequence-specific DNA and protein molecules. As theoretical biologist Howard Pattee explains, "There is no evidence that hereditary evolution [natural selection] occurs except in cells which already have ... the DNA, the replicating and translating enzymes, and all the control systems and structures necessary to reproduce themselves." But this fact of molecular biology posed an obvious difficulty for Oparin's theory of prebiotic natural selection. In order to explain the origin of specified information in DNA, Oparin invoked a process that depends on preexisting sequence-specific (i.e. information-rich) DNA molecules. Yet the origin of these molecules is precisely what his theory needed to explain. As Christian de Duve explains, theories of prebiotic natural selection necessarily fail because they "need information which implies they have to presuppose what is to be explained in the first place." (Signature, pp. 274-275.)

There is no analogous justification for ruling out intelligent design. You’ve certainly offered none, other than “fair is fair.” You appear to be using a contrived definition of “fair,” because you’ve offered no principled reason for excluding ID. Your exclusion of ID appears to be arbitrary, based upon a distaste for the ID conclusion. In fact, I can offer a justification for why we can suspect that intelligent agency existed prior to the origin of life.

The fine-tuning of the universe shows powerful evidence of design. That fine-tuning was in place when the universe first came to exist, some 13 billion years ago. That’s some 8-9 billion years prior to the origin of life on earth. So we have pretty good reasons to believe that intelligent agency existed, and was influencing the universe, prior to the origin of life on earth.

You have a very strange notion of “fair”.

Nick wrote: “It is clear that the quote Meyer uses over and over and over, entirely uncritically, to the effect that ‘prebiotic natural selection is a contradiction in terms’, is a decades-old oversimplification at best. Modern research does not conclude this -- see for example this prominent paper which Meyer somehow, mystifyingly, missed: Martin A. Nowak and Hisashi Ohtsuki (2008). "Prevolutionary dynamics and the origin of evolution." Proceedings of the National Academy of Sciences, 2008 Sep 30;105(39):14924-7. Epub 2008 Sep 12. )”

I reply: This paper actually acknowledges that Meyer’s thinking is quite “normal,” as it states: “Evolution needs mutation and selection. Normally, one thinks of these properties as being derivative of replication…” Of course the paper goes on to claim that you can have mutation and selection without replication.

And if you read the paper carefully to see what they’re saying, they haven’t really removed replication from the situation. They’ve just redefined the meaning of replication, where they speculate that perhaps some reactions tend to produce certain sequences more often than others. Basically, their argument amounts to this: If (for no apparent reason other than the fact that it just happens) some reactions happen more than others leading to sequences of monomer, then some sequences will accumulate at a greater rate than others.

Then they “assume that some sequences can act as a templates [sic] for replication,” and of course those can make even more copies of themselves and you have the phase transition from “prelife” to “life.” In their scheme, replication has arisen for no apparent reason, but there is no reason why these accumulating molecules should select for the trait of self-replication. This is the problem that Meyer notes for prebiotic causes: there is no reason to generate information. It’s just assumed that information arises by chance, out of sheer dumb luck.

In fact, they are confusing Shannon information with complex and specified information. In their scheme, long sequences of 0s and 1s accumulate (for no apparent reason) but there’s also no reason to think that they will be arranged in a pattern that carries any meaning, or performs any function. Their scheme might generate Shannon information, but not complex and specified information. So it's not going to generate the kind of information of interest to those seeking to understand the origin of life's functional complexity.

It’s also noteworthy that this is a completely theoretical paper, with no references to the real-world of chemistry. So basically, their argument is this: If you ignore all the realities of chemistry (such as severe problems encountered naturally polymerizing monomers into long polymer strings outside of the biological context), and assume that some reactions will generate certain strings of monomers more than others, and then assume that some strings of monomers just happen to be capable of self-replication, then we can produce life. I see a lot of assumptions that require no assent, and no references to the real world. Sure, they work out the population dynamics under their hypothetical processes and assumptions, but there’s no evidence those hypothetical processes and assumptions have any bearing upon the real world.

At least Darwinian evolution relies on a biologically observed process to produce more copies of certain individuals (e.g. reproduction/replication) but this paper invents some speculative process that isn’t observed in the real world, and claims that it can be a substitute for replication. I suppose it’s easy to have natural selection without replication when you don’t have to conform your argument to anything in the real world.

You call it “mystifying” that Meyer didn’t mention this paper from PNAS, but given that it proposes no real-world chemical analogy for its ‘presto, imaginary and hypothetical chemical reactions might produce more of one molecule than another, which might eventually lead to information, which might eventually lead to biological replication, all for no apparent reason’ argument, I don’t see why it deserved much attention.

Nick wrote: In a later post, Luskin writes,

"Is it persuasive to invoke natural selection as the cause of new genetic information when you don’t even know what function is being selected? This is why I said that in many cases, natural selection is used as a “magic wand.” It’s just asserted, even though no one has established what was really going on."

Oh really? So your position is that if we don't know everything, we know nothing, I guess, and can safely infer that no such thing could have ever possibly occurred? And we can then safely infer that it must have been divine intervention that produced Sdic?

I reply: From looking at what you quoted from me, this badly misrepresents my position. As I’ll discuss below, you have a knack for misconstruing ID positions and reframing the issue in an unfair manner to suit materialism. My position is not “if we don't know everything, we know nothing”. Rather, my position is the far more reasonable: “if we don't know anything, we know nothing.” If you claim that natural selection was at work, and you don’t even know what function was being selected, then you don’t know very much, and you certainly haven’t demonstrated natural selection was at work. Austin Hughes agrees:

A major hindrance to progress has been confusion regarding the role of positive (Darwinian) selection, i.e., natural selection favoring adaptive mutations. In particular, problems have arisen from the widespread use of certain poorly conceived statistical methods to test for positive selection. Thousands of papers are published every year claiming evidence of adaptive evolution on the basis of computational analyses alone, with no evidence whatsoever regarding the phenotypic effects of allegedly adaptive mutations. … Contrary to a widespread impression, natural selection does not leave any unambiguous ‘‘signature’’ on the genome, certainly not one that is still detectable after tens or hundreds of millions of years. To biologists schooled in Neo-Darwinian thought processes, it is virtually axiomatic that any adaptive change must have been fixed as a result of natural selection. But it is important to remember that reality can be more complicated than simplistic textbook scenarios. … In recent years the literature of evolutionary biology has been glutted with extravagant claims of positive selection on the basis of computational analyses alone ... This vast outpouring of pseudo-Darwinian hype has been genuinely harmful to the credibility of evolutionary biology as a science.

(Austin L. Hughes, "The origin of adaptive phenotypes," Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193–13194 (Sept. 9, 2008) (emphasis added) (internal citations removed).)

Like Hughes, ID proponents are also aware that the phenotypic effects of mutations is determinative of whether they will be preserved and accumulate. (See the discussion of Axe’s work above.) So when Darwinian evolutionists assert that random mutation natural selection occurred, but ignore the phenotypic effects of those mutations and whether they would be preserved by selection, then they have not demonstrated that natural selection could have produced the trait in question.

But the case of Sdic doesn’t even go that far: they don’t even know the trait in question that we’re selecting for, much less whether intermediate steps would be preserved by selection. Here’s a far more accurate description of what’s really going on here: Rather than me suggesting we can’t infer selection until we know everything, we actually see Nick Matzke suggesting we should infer selection when we know virtually nothing.

Nick wrote: “it *implausible* that natural selection spread a gene like Sdic to fixation?”

I reply: If the gene Sdic already exists, and it provides a strong selective advantage, then it’s probably not implausible for such a trait to be fixed into a population. But you’ve changed the subject Nick, because fixing a gene isn’t what we’re talking about. We’re talking about producing a gene so it can be fixed in the first place.

Natural selection can only preserve features produced by mutations. If mutations cannot produce the feature in question, then it will not be available for natural selection to preserve. Asking whether a fully-functional-and-advantageous gene can become fixed in a population is a relatively trivial question, and an entirely different question from asking whether the fully-functional-and-advantageous gene can arise in the first place.

Your framing of the issue dodges the important question here.

Nick wrote: “With Sdic, we have the ancestral sequences of the (two) genes that were partially copied and fused to produce Sdic. Sdic currently lives between these two genes. Sdic exists in 4 copies IIRC, and we can identify all the point mutations that separate it from its ancestor.”

I reply: It would help if you could provide a citation to back these claims, but let’s assume for the sake of argument that everything you say is true. Great! What we really have are homologous sequences which are assumed to have been “ancestral.” Perhaps they were, perhaps they weren’t. I’m not saying it’s impossible. I’m saying that we should test these claims and demonstrate a plausible stepwise evolutionary pathway to produce these genes.

My attitude here isn’t eager to refute Darwinian evolution; it’s eager to seek truth. Are you open to the possibility that gene duplication+mutation+selection is wrong?

Nick, you are framing my argument as if I’m saying it’s “implausible” that this happened. You’re putting words in my mouth. I’m not necessarily saying that. What I’m saying is that we should test claims of Darwinian evolution for plausibility before we assert that they are plausible. You are claiming they are “plausible” without having demonstrated that there is a stepwise evolutionary pathway.

Identifying necessary point mutations is a good start. Now, let’s ask questions like:
“what advantages might these point mutations have given?”
“can they provide a stepwise advantage?”
“are there instances where multiple mutations are required to produce an advantage?”
“are such multi-mutation steps likely to arise given known mutation rates and generation times?”


You frame this as if I'm demanding that we “know everything,” but I’m just suggesting we should seek truth and not assume that the answers to these questions will always be favorable or Darwinian processes. Why are you so eager to infer Darwinian evolution Nick when you don’t really know if it’s a scientifically plausible explanation? What’s the harm in seeking truth?

Maybe it will turn out that Sdic could have arisen by mutation and selection through a series of stepwise mutations. Maybe it won’t. I’m open to the possibility, but I’m under no compulsion to accept claims that it did when we just don’t know.

In fact, some aspects of the story behind Sdic make me very skeptical. For example, consider this aspect of the Sdic story:

First, although a testes-specific promoter was essential for Sdic, this unusual regulatory region did not really “evolve.” Instead it was aboriginal, created de novo by the fortuitous juxtaposition of suitable sequences. The more extensive evolutionary changes took place in Cdic intron 3, enabling an originally untranslatable sequence to become a new coding region whose product functions in the assembly of axonemal dynein.

(Dmitry I. Nurminsky, Maria V. Nurminskaya, Daniel De Aguiar, and Daniel L. Hartl, “Selective sweep of a newly evolved sperm-specic gene in Drosophila,” Nature, Vol. 396:572-575 (December 10, 1998). )

So the regulatory region “did not really ‘evolve’” but was spontaneously “created de novo by the fortuitous juxtaposition of suitable sequences”. What are the odds of that happening by chance? They don’t seem very good. So why would you accept that they did happen when it hasn’t been demonstrated that such events are scientifically plausible?

Nick wrote: “Furthermore, Sdic exists right in the middle of a region of reduced heterozygosity in the Drosophila genome, which is exactly the statistical pattern that you expect from a selective sweep.”

I reply: A selective sweep just means that the allele in question is unbiquitous throughout a population. Some selection pressure and/or a bottleneck is then inferred, but as far as the hard data goes, all you really have observed is this: the trait is extremely common (if not ubiquitous) in the population. So what? Again, the question is not whether a highly advantageous allele can become fixed in a population. It’s how the allele can arise in the first place.

Nick wrote: We know that Sdic is expressed strongly in sperm cells, unlike the ancestors IIRC. And, furthermore, there is lot of a priori evidence and theory that suggests that genes targeted to sperm should evolve rapidly and will be under strong selection (seeing as the options for a gene variant in a sperm cell is to either fertilize an egg or die trying and be lost from the gene pool forever).”

I reply: Great—that’s a tiny little start, but a good one! We know that Sdic probably has some function pertaining to reproduction. But what is that function? What exactly is the function of Sdic? What function as being selected for? What selective advantages did mutations offer? What are the odds of those mutations happening? Could they happen within the available timescale? Contra Nick’s claims, I’m not saying that Sdic couldn’t have arisen by natural selection and random mutation: what I’m saying is that you haven’t established that it is plausible that it did.

Nick wrote: “All of this adds up to an extremely reasonable case that Sdic made some advantageous modification to the sperm, probably effecting motility (since dic = dynein intermediate chain), and was thus swept to fixation. What is *unreasonable* or *magical* about this hypothesis?”

I reply: There’s nothing unreasonable about this hypothesis. It just doesn’t demonstrate Darwinian evolution occurred.

Nick wrote: “Are we really supposed to take seriously the idea that an "Intelligent Designer", slash God, has been monkeying around with Drosophila sperm genes?”

I reply: When the evidence is not on your side, you resort to mockery and ridicule, right Nick?

Nick wrote: “If you can't show that the natural evolution of Sdic and similar cases is *unreasonable* and *implausible*, then you cannot argue that it is *implausible* to think that natural evolution can produce new genes, and thus substantial amounts of new information.”

I reply: Again, you are putting words in my mouth Nick: I’m not saying the Darwinian evolution of Sdic is impossible, just that it hasn’t been demonstrated to be plausible in this case. We simply don’t know that the evolution of Sdic is plausible because no one has determined important things like the following:

(a) the function of Sdic
(b) the function being selected for at each step of Sdic’s evolution
(c) a stepwise series mutations which could produce Sdic
(d) whether those mutations provide a stepwise advantage
(e) whether any steps require multiple mutations to provide an advantage
(f) whether this pathway is likely to occur in a reasonable timescale.

No one has even completely addressed item (a), and yet you expect me to believe that the evolution of this gene is plausible? I’m just asking that we demonstrate that the Darwinian evolution of Sdic is plausible before we declare it is. Why is that so unreasonable?

You want us to infer natural selection when we don’t even know what function is being selected for. Who now is being “unreasonable”?

And if Sdic could arise by natural selection and random mutation, that doesn’t therefore show that all genes can arise by natural selection and random mutation. Perhaps there’s a plausible pathway of stepwise mutations leading to Sdic. No one knows that there is, but perhaps there is. If there is, that doesn’t mean that all genes are like Sdic.

Your logic reflects how evolutionists are often over-eager to extrapolate from one case to all cases. We know that there are barriers to Darwinian evolution when multi-mutation steps are encountered, so you can’t assume that just because such barriers don’t exist in one case, that therefore they don’t exist in all cases.

Again Nick, you have a knack for misrepresenting ID arguments and reframing the issue in an unreasonable manner.

Nick wrote: “And if you can't argue that, then Meyer's argument that intelligence is the only known cause of meaningful amounts of information collapses.”

I reply: Let me get this straight: If I don’t assent to your claims that a gene evolved by natural selection and random mutation, when we haven’t even determined what function was being selected for (much less addressing any of the other crucial matters above) then Stephen Meyer’s argument (which only applies to prebiotic chemical evolution, and not biological evolution) is flawed? This makes no sense.

Nick wrote: “Arguing that we don't know every last detail of any particular case doesn't get you there, by a long shot.”

I reply: This reframing misses and misconstrues what’s really going on here. I’m not saying that we know for a fact that Sdic couldn’t have evolved. What I’m saying is that you don’t know that it could have evolved. We don’t know that there aren’t severe barriers to the evolution of Sdic. What are the odds that its promoter region was spontaneously “created de novo by the fortuitous juxtaposition of suitable sequences”? You haven’t shown that it’s plausible.

There’s a big difference.

Nick wrote: “The explanation we have for the origin of Sdic is incredibly detailed as it stands … No one has produced a better, more detailed explanation”

I reply: Wow: You just admitted that the most “detailed explanation” for the evolution of a gene represents a case where:

they don’t even know the precise function of the gene,
and thus don’t know what function was being selected,
and thus don’t know if there are steps that require multiple mutations to produce an advantage,
and thus haven’t even begun to show that the gene can evolve in a step-by-step fashion,
and thus don’t know that there are sufficient probabilistic resources to produce the gene by gene duplication+mutation+selection.

In effect, you have just admitted that Darwinian explanations for the origin of genes are incredibly detail-poor.

Nick wrote: “Science demands hypotheses that are detailed enough to be testable, preferably statistically testable, and the more details you have, the more precise tests you can make.”

I reply: I agree. Then I suppose that the claim that Sdic evolved by Darwinian evolution is not scientific because no one appears interested in actually testing whether stepwise mutations can actually produce the gene in question.

Do you think that it is plausible to claim that part of a gene was “created de novo by the fortuitous juxtaposition of suitable sequences”?

Nick wrote: “I challenge the ID proponents: produce an ID explanation of Sdic that is as detailed and well-evidenced as the evolutionary one.”

I reply: I’m tempted to say “That shouldn’t be very hard, given the lack of details.” But in all seriousness, Nick is again framing the issue wrong.

The measure isn’t “whose explanation is more detailed?” The measure is, “whose explanation is causally adequate?”

Now perhaps Darwinian evolution will turn out to be causually adequate to explain Sdic. So far, Darwinian evolutionists have done a pretty poor job of making their case. But perhaps someday they will.

Is ID causually adequate? ID proponents have observed:

"Agents can arrange matter with distant goals in mind. In their use of language, they routinely 'find' highly isolated and improbable functional sequences amid vast spaces of combinatorial possibilities." (Stephen C. Meyer, "The Cambrian Information Explosion," in Debating Design (edited by Michael Ruse and William Dembski; Cambridge University Press 2004).)
"[W]e have repeated experience of rational and conscious agents-in particular ourselves-generating or causing increases in complex specified information, both in the form of sequence-specific lines of code and in the form of hierarchically arranged systems of parts. ... Our experience-based knowledge of information-flow confirms that systems with large amounts of specified complexity (especially codes and languages) invariably originate from an intelligent source from a mind or personal agent." (Stephen C. Meyer, "The origin of biological information and the higher taxonomic categories," Proceedings of the Biological Society of Washington, Vol. 117(2):213-239 (2004).)
"Intelligent design provides a sufficient causal explanation for the origin of large amounts of information, since we have considerable experience of intelligent agents generating informational configurations of matter." (Stephen C. Meyer, Marcus Ross, Paul Nelson & Paul Chien, "The Cambrian Explosion: Biology's Big Bang," in Darwinism, Design, and Public Education (John A. Campbell and Stephen C. Meyer eds., Michigan State University Press, 2003).)

ID is causally adequate to produce exactly the sort of complex and specified DNA code which is required to produce functional genes. In contrast, it hasn’t been demonstrated that Darwinian evolution is a causally adequate explanation. After all, Nick just admitted that in the most “detailed explanation” for the origin of a gene by Darwinian evolution, we don’t even know the function of the gene, and don’t know what function was being selected for.

In closing, Nick, you have a knack for framing issues to suit the Darwinian position, but not to foster the objective search for scientific truth:

You argue that if logic excludes natural selection from prebiotic processes, then it’s “fair” to exclude intelligence from the same, even though you provide no ID-specific reason for excluding intelligence.
If a paper with no references to the real world of chemistry asserts that unguided chemical reactions can produce information by preferring certain long sequences of monomers (for no apparent reason), and then “assumes” that somehow those for-no-apparent-reason strings of monomers are capable of self-replication, then Steve Meyer is wrong and it’s “mystifying” that he wouldn’t take the time to rebut the argument.
You misconstrue my position that asks proponents of natural selection to at least explain what function is being selected to imply I’m expecting proponents of natural selection to provide “infinitely detailed explanations.”

You're welcome to frame the issues as you like. But I think that fair-minded readers will see that your framing of the issues doesn’t address ID arguments, and is suspiciously suited to favor Darwinian evolution, not fairness and the objective search for scientific truth. Here’s what’s I think is really going on:

You are trying to exclude ID arbitrarily from science
You have provided a citation bluff to claim that information can arise by mutation and selection in a pre-biological context
You have mischaracterized my reasonable request for minimal detail in Darwinian explanations as a demand for “infinitely detailed explanations”

And at the same time, you’ve admitted that the most “detailed explanation” of the Darwinian origin of a gene entails a case where we don’t even know what function is being selected for, and evolutionists were forced to appeal to its promoter region having been “created de novo by the fortuitous juxtaposition of suitable sequences.” That's quite a weighty admission on your part which doesn't bode well for Darwinian explanations.

In closing, you frame your response to me as pointing out things that I "missed". I don't see how I failed to respond to any rebuttal you had made, but I can't help but note that you in fact have not responded to my other comment which points out how you misrepresented my arguments about the evolution of new genetic information by claiming my "only response" was to equate Darwinian explanations with "magic." Thanks.

Casey

p.s. while we’re on the topic of magic, for the record, I'm not the first person to criticize vague appeals to natural selection as looking like "magic". Carl Woese writes:


The creation of the enormous amount and degree of novelty needed to bring forth modern cells is by no means a matter of waving the usual wand of variation and selection. What was there, what proteins were there to vary in the beginning? Did all proteins evolve from one aboriginal protein to begin with? Hardly likely! (Evolution’s rule, to which there are, fortunately, a few exceptions, is that “you can’t get there from here.”) Our experience with variation and selection in the modern context does not begin to prepare us for understanding what happened when cellular evolution was in its very early, rough-and-tumble phase(s) of spewing forth novelty. (Carl R. Woese, "A New Biology for a New Century," Microbiology and Molecular Biology Reviews, Vol. 68(2): 173–186 (June, 2004) (emphasis added).)

And since we're talking about BioLogos here in this article, it's worth noting that another prominent BioLogos biologist, Kathryn Applegate, has stated "Natural forces work 'like magic'." (For the details, see here.) Is it OK for ID critics to use terms like "magic" when describing unguided processes, but not for an ID proponent to do the same?

If Jon Watts is going to refute Meyer’s law of conservation of information, then he’s going to have to account for the fact that it was explicitly formulated to apply in a non-biological context—to the origin of information in the first life through non-biological processes. If Jon Watts wishes to cite experiments showing how biological information can arise through unguided chemical and physical processes, that’s great and it would meet Meyer’s thesis! But Jon Watts is not doing that.

OK, here goes. In vitro selection experiments can also lead to new information in a non-biological context. Interested readers can look up "in vitro selection" or "SELEX" for examples. The core of a SELEX experiment is that a pool of oligonucleotides (short pieces of DNA or RNA) of random sequence are sorted (selected) according to their function - the one that carries out that function the best is saved. We have zero complex specified information at the beginning of the experiment (the pool of random-sequence pieces of DNA), but by the end we have a single oligonucleotide whose specific sequence (specified information) gives it a desirable set of properties.

To name one of many examples, the FDA-approved drug Macugen was derived from such a process.

This is not a simulation of the origin of life, or of biomolecules in the first place. But to me it is a clear example of information arising in a non-biological context.


I am glad to find intelligent people arguing for intelligent design.
Now, could we please have only non-intelligent people arguing for non-intelligent design?......PLEASE!
Intelligent people are not qualified to represent time and chance non-intelligent design. How would they know it's capabilities or its limitations? They are intelligent, and thereby incapable of knowing whether non-intelligence is capable of anything, let alone producing intelligence.
An intelligent argument for non-intelligence is an oxymoron.

From all the debates I’ve watched on Youtube and brush readings of various blogs, what comes through clearly is that both sides interpret the data according to their premise. And one has to admire how the likes of Ken Miller juggle the data to come up with some fairly plausible counter arguments against design. We see that here too, as Casey’s arguments are apparently dismissed with a few deftly keystrokes. Papers and experiments are cited which onlookers have no hope to Google let alone understand.

Across the pond, the mental gymnastics Richard Dawkins puts on display for the BBC and Channel 4 crowd, as he reasons in behalf of Evolution, is a phenomenon in itself. We are not dealing with Apologists or even simple Scientist but sleek Lawyer Advocates for Darwin! The reasonings employed in the debate, the counter arguments, is what a high flying corporate attorney would utilise. No wonder it all sounds plausible, the waving away of the data and dismissive brashness. But debates quickly leave the Science behind, within a few lines and sentences as it boils down to how the data is interpreted; and the spectre of the Theological implication rises.

The only way Darwin’s Theory can survive this trial, is that it can be shown that at the molecular level, the influence of Quantum Mechanics is stronger than was previously thought. It seems to me that the only way to get around the limitations of Random Variation is to redefine what “Random” means. If it’s a case that more probabilistic “forces” are coming into play, and that the weird, non-intuitive realm of the subatomic are generating the specified information, then that would return the all of this to equilibrium. The problem there of course is that, Darwin’s advocates will have to learn some heavy duty mathematics, a subject Darwin himself wasn’t too confident about.

Failing that, ID wins the debate since fundamentally is has logic on its side. Regardless of the Theological implications, random unguided events cannot generate Specified Information. And DNA is extremely specified.

Hello again Nick- You've missed a couple points, I'm afraid-

1- Again with the equivocation as ID is not anti-evolution, raher ID says some or even most genetic changes are not by chance.

2- The origin of life- as in your example of the sdic gene is using existing biological organisms and therefor once again BEGS THE QUESTION. It could very well be that the scenario described at your link was via some targeted search.

A collection of NEW information that is useless and makes no sense is a severe dis-advantage. Gradually add up useless information and see what happens.

Really, how is this different than the size of finch beaks that Darwin observed? Recall that during environmental changes, the size of finch beaks changed to ensure the birds' survival. Also recall that when environmental conditions switched back to normal, the finch beaks went back to normal as well. There's really nothing new here: the information is already present in the organism. Environmental changes simply coax out that information.

This seems to be a rather well designed system; one that is able to adapt and change to compensate for unexpected threats in environmental conditions.

Thank you, you really write in a way everyone - including me :-) - can@is able to understand, even if someone is not so familiar with these things. But what exactly do you mean with your third paragraph? Frank

That is so interesting:

“The belief that Darwin’s Theory somehow saves mankind from superstition”

“All genuine Scientists are somehow duty bound to defend natural selection acting on random variation”

That was OK in 1995 when we had scientists saving us from “the demon-haunted world”. That was then and this is now, and now we hear only the voice of ideologues. The Darwinian establishment has been hollowed out.

• Ideology is certainly easier to generate than “ground-breaking and new science”.

Natural selection cannot deal with “irreducible complexity” or the “nature of a system”. In “all” functioning systems the whole is greater than the sum of the parts.

ALL of “this” has become ideological, the establishment, are now ideologues only, and they plead a case for “silence”, and they do not know good science, and they can no longer compete in the scientific arena!

Intellectually, the ID coalition of scientists is accelerating away from what is left of the neo-Darwinian confederation of scientists. Things are moving faster in the world of science than the old establishment to prepared to deal with.

- RFP

Oh just wait!

There will be a multitude of people arguing that evolutionary theory has not been
falsified because...


1. We didn't use the right microbial strain.

2. Different test conditions would've produced better results.

3. The experiment just needs a little more time.

4. Evolution never had a "goal" of producing new information, but it could.

5. There must be some kind of multiverse to give enough trials.


...all while simultaneously claiming that ID is untestable and has already been falsified.

The Naturalist is forced to compromise his "Scientific" ideal at many junctures in order to maintain his religious belief.
The biopolymers required for life breakdown unless living components build them up. Is this not a law of chemistry?
Contrary to this current evidence, naturalist religion requires you to believe that the biopolymers required for life were built up with no living help and then came to life.
Its magician verses magician in this debate. "POOF"

Hi Nick,

Seeing that ID is not anti-evolution your response is disingenuous at best. The argument is that blind, undirected chemical processes cannot create biologically functional systems, ie biological information, where those systems don't already exist.

By using gene duplication followed by mutation you are engaging in question-begging, eg "Are gene duplications blind and undirected?" Dr Lee Spetner wrote a book about that- "Not By Chance"- and that is what ID says- not by chance and your position is all about happening by chance.

With respect to Jingwei, their first inference of positive selection were indepedent tests like McDonald-Kreitman tests and HKA. Then they found higher relative catalysis rates for two substrates(geraniol, farnesol) involved in pheromone metabolism, while the parental gene, ADH, used ethanol as a substrate.

The thing I 'like' about ID is that the ID scientist use valid data in coming to a conclusion, while most Neo-Darwinist's rely on assumptions to try to further prove their unproven point. While I hear many times that ID is NOT based on science, I often find it the other way around in most cases, that Natural Selection is based solely on unproven, "assumptions" and that it's ID that will eventually 'show' whether Natural Selection has the ability OR not to invent something new that never existed before in the original!

To me, given two physical attributes in two different living 'things', added together will always be the just these two attributes added together in the new living 'thing' but the new living 'thing' will never show a "NEW" attribute that was never seen in the two original 'things' from which it came... This is just an "assumption" that a new attribute came about and I have never seen any proof that a new attribute came about by combining two other, non-related attributes. So while IDers rely on finding this proof, Neo-Darwinians rely on assumption that it must have happened all because of the diversity of life that exists.

To me, this diversity that we cannot yet show happened by Natural Selection only helps to 'prove' the stance that life did NOT evolve in the manner that Darwin outlined and that many people that believe in such a stance base all their beliefs of such, in unproven 'assumption'!

My hat's off to the field of ID and the actual science and hard work that goes into actually trying to 'prove' Natural Selection and in not being able to prove such a stance, shows that the stance of Natural Selection must be flawed in the way that most people study and teach it. Just saying...

I appreciate that some scientists have taken the time to document their findings in order to provide true scientific arguments against politically correct arguments. In today's culture, they may be risking loss of reputation, scolding, ridicule, and diminished number of job offers.

Dear Readers,

This comment will reply to the rest of Nick Matzke’s comment that I didn’t reply to in my prior comment. As we saw in my prior comment, Nick Matzke wrote:

Luskin's only response to this work has been a post that claims that inferring gene duplication, point mutations, and natural selection to explain the sequence and diversity features we see when examining e.g. a series of gene sequences that are obviously copies of each other with more or less modified sequences has been to call the invocation of these these well-known, well-documented processes no better than ‘waving a magic wand’.”

This is actually a very instructive comment from Nick, and I’m glad he made it. But it’s probably not instructive in the way Nick intended it.

ID proponents have long-experienced that many critics misrepresent, misconstrue, and ignore our arguments. This led William Dembski to aptly observe:

Our critics have, in effect, adopted a zero-concession policy toward intelligent design. According to this policy, absolutely nothing is to be conceded to intelligent design and its proponents. It is therefore futile to hope for concessions from critics. This is especially difficult for novices to accept. A bright young novice to this debate comes along, makes an otherwise persuasive argument, and finds it immediately shot down. Substantive objections are bypassed. Irrelevancies are stressed. Tables are turned. Misrepresentations abound. One's competence and expertise are belittled. The novice comes back, reframes the argument, clarifies key points, attempts to answer objections, and encounters the same treatment. The problem is not with the argument but with the context of discourse in which the argument is made. The solution, therefore, is to change the context of discourse.Hardcore critics who've adopted a zero-concession policy toward intelligent design are still worth engaging, but we need to control the terms of engagement. Whenever I engage them, the farthest thing from my mind is to convert them, to win them over, to appeal to their good will, to make my cause seem reasonable in their eyes. We need to set wishful thinking firmly to one side. The point is not to induce a cognitive shift in our critics, but instead to clarify our arguments, to address weaknesses in our own position, to identify areas requiring further work and study, and, perhaps most significantly, to appeal to the undecided middle that is watching this debate and trying to sort through the issues.(William Dembski, "Dealing with the Backlash Against Intelligent Design" (April 14, 2004).)

This is the context we’re dealing with here in engaging Nick Matzke. For those who are interested, here’s what’s happening:

I didn’t say anything about “magic” in my article here. So why is Nick talking about some comment I made about “magic” quite a while back? He wants to claim it encapsulates my criticisms and is my “only response” to claims of the evolution of new genes. I’m happy to let fair-minded readers decide if Nick is correct.

Yes, I’ve used that the word “magic” a couple times before, but only in a certain context: I used it at a couple points in a 10,000+ word essay, The NCSE, Judge Jones, and Citation Bluffs About the Origin of New Functional Genetic Information, which cited dozens of mainstream scientific papers, and showed that many accounts of the Darwinian evolution of genes are unpersuasive.

To illustrate why I used the word “magic,” we often see that papers (which Nick would probably claim show the “origin of new genetic information”) invoke natural selection, but then:

do not identify a stepwise mutational pathway,
do not identify what advantages might be gained at each step
do not calculate the plausibility of this pathway evolving under known population sizes, mutation rates, and other relevant probabilistic resources, and in many cases
DO NOT EVEN KNOW THE FUNCTION OF THE GENE, AND THUS HAVE NO IDEA WHAT FUNCTION WAS BEING SELECTED FOR

(For example, the following papers invoke natural selection to explain the origin of a gene whose function was at-the-time unknown, meaning they did not even know what function was being selected: Manyuan Long & Charles H. Langley, “Natural selection and the origin of jingwei, a chimeric processed functional gene in Drosophila,” Science, Vol. 260:91–95 (April 2, 1993); Dmitry I. Nurminsky, Maria V. Nurminskaya, Daniel De Aguiar, and Daniel L. Hartl, “Selective sweep of a newly evolved sperm-specic gene in Drosophila,” Nature, Vol. 396:572-575 (December 10, 1998); David J. Begun, “Origin and Evolution of a New Gene Descended From alcohol dehydrogenase in Drosophila,” Genetics, Vol. 145:375-382 (February, 1997); Jianzhi Zhang, David M. Webb and Ondrej Podlaha, “Accelerated Protein Evolution and Origins of Human-Specific Features: FOXP2 as an Example,” Genetics, Vol. 162:1825–1835 (December 2002); Esther Betran and Manyuan Long, "Dntf-2r, a Young Drosophila Retroposed Gene With Specific Male Expression Under Positive Darwinian Selection," Genetics, Vol. 164:977–988 ( July 2003).)

Is it persuasive to invoke natural selection as the cause of new genetic information when you don’t even know what function is being selected? This is why I said that in many cases, natural selection is used as a “magic wand.” It’s just asserted, even though no one has established what was really going on.
After my essay offered extensive analyses of multiple papers purporting to explain the origin of new genes, I conclude:

In not a single case did the above papers cited by Long et al. actually explain how new functional information arose. In no case was there an analysis of how natural selection could have favored mutational changes that were shown to be likely along each step of an alleged evolutionary pathway; never was any detailed step-by-step mutational pathway even given. At best, these studies offered vague and ad hoc appeals to duplication, rearrangement, and natural selection — often in a sudden, extreme, and abrupt manner — to form the gene in question. In many cases, natural selection was invoked to allegedly account for changes in the gene, even though the investigators didn’t even know the function of the gene and thereby could not identify the advantage provided by the gene’s function. In no case were calculations performed to assess whether sufficient probabilistic resources existed to produce the asserted mutational events on a reasonable timescale. In some cases, the original genetic material for the genes was unknown, or the studies asserted spontaneous “de novo” origin of genes from previously non-coding DNA. While they readily admitted that “de novo” gene emergence is rare, no attempt was made to assess whether such an unguided mechanism is even remotely plausible on mathematical probabilistic grounds. These papers play the Gene Evolution Game, but never ask the right questions to explain how neo-Darwinian mechanisms create new genetic information.

The NCSE’s (and Judge Jones’s) citation bluffs have not explained how neo-Darwinian mechanisms produce new functional biological information. Instead, the mechanisms invoked in these papers are vague and hypothetical at best:
exons may have been “recruited” or “donated” from other genes (and in some cases from an “unknown sou[r]ce”);
there were vague appeals to “extensive refashioning of the genome”;
mutations were said to cause “fortuitous juxtaposition of suitable sequences” in a gene-promoting region that therefore “did not really ‘evolve’”;
researchers assumed “radical change in the structure” due to “rapid, adaptive evolution” and claimed that “positive selection has played an important role in the evolution” of the gene, even though function of the gene was not even known;
genes were purportedly “cobbled together from DNA of no related function (or no function at all)”;
the “creation” of new exons “from a unique noncoding genomic sequence that fortuitously evolved” was assumed, not demonstrated;
we were given alternatives that promoter regions arose from a “random genomic sequence that happens to be similar to a promoter sequence,” or that the gene arose because it was inserted by pure chance right next to a functional promoter.
explanations went little further than invoking “the chimeric fusion of two genes” based solely on sequence similarity;
when no source material is recognizable, we’re told that “genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors” because they are simply “hypermutable”;
we even saw “a striking case of convergent evolution” of “near-identical” proteins.
To reiterate, in no cases were the odds of these unlikely events taking place actually calculated. Incredibly, natural selection was repeatedly invoked in instances where the investigators did not know the function of the gene being studied and thus could not possibly have identified any known functional advantages gained through the mutations being invoked. In the case where multiple mutational steps were involved, no tests were done of the functional viability of the alleged intermediate stages. These papers offer vague stories but not viable, plausibly demonstrated explanations for the origin of new genetic information.

(The NCSE, Judge Jones, and Citation Bluffs About the Origin of New Functional Genetic Information)

Here is Nick Matzke’s style of debate: he takes my extensive analysis and caricatures it as if my “only response” is that supposed mechanisms of genetic evolution are “no better than ‘waving a magic wand’.”

The above is just a snippet of the total essay (there’s a lot more analysis in my essay, for those who care to read it), but it seems like I said a lot more than calling evolutionary explanations "magic". But Nick says that calling them "magic" is my "only response." Does Nick accurately state my arguments?

Forgive me Nick, but I have trouble accepting claims of natural selection when evolutionary biologists:

(a) don’t even know the function that is being selected,
(b) haven’t demonstrated what advantages might have been gained along each step,
(c) haven’t demonstrated steps in an alleged mutational pathway, and / or
(d) haven’t shown that the purported pathways are mathematically plausible.

Perhaps for Mr. Matzke, he has enough faith to accept natural selection as an explanation when all of those necessary components of an evolutionary explanation are completely ignored. Personally, I don’t have that much faith, and Darwinian evolution is not "obviously" the cause when these important issues go completely unaddressed. Some other evolutionary biologists feel something like I do, such as Austin Hughes, who warns against “statistically based claim[s] of evidence for positive selection divorced from any biological mechanism” (see here and here for a discussion).

Ironically, while Nick attacks me for calling such evolutionary claims no better than “waving a magic wand,” in the same breath he then calls ID “magic”, and without any analysis or discussion, he simply caricatures, labels, and mischaracterizes ID as a “poof” hypothesis. This is why I feel Nick Matzke’s comment is instructive, as it shows the unsophisticated, unfair, and inaccurate style of his criticisms of ID.

In closing, I’m happy to let readers decide if Nick Matzke has responded to my arguments by claiming that my “only response” to claims of genetic evolution is that they amounts to “magic.” Has Nick accurately stated my arguments?

Thanks for reading.

Sincerely,

Casey

Dear Jon Watts and Nick Matzke,

Thanks to both of you for coming and participating. I'd like to reply to you both with one comment.

Jon Watts wrote: “Venema was responding to a specific claim that Meyer makes in Signature (and Dembski made a decade earlier) - namely the law of conservation of information. If ID is going to make claims in the form of a law - that information does not ever arise without direct intelligent input - then it is a sufficient, appropriate critique to show that one or more counterexamples exist.”

And Nick Matzke suggested that “Casey Luskin's entire series of posts is devoted to obscuring and avoiding dealing with this critical issue.”

I think that the commenter “IDEvo” responded to Jon Watts quite well with this comment:

“I guess that settles it then. If you [Jon Watts] say so, it must be so. You don't have to give any examples. We'll just take your word for it.”

I suppose the same could be said in response to Nick Matzke when he asserts there are “numerous, extremely well-documented…cases of evolution creating new genes with new functions”—but then also provides no examples.

Well, Dennis Venema did better than Jon Watts and Nick Matzke because at least he tried to give some examples. But there are some problems with Venema’s arguments:

Problem 1: The first problem is that the examples Venema offers did not demonstrate new genetic information arising in the form of, as Meyer asks for it, “fundamentally new genes and proteins.” (p. 494)

Problem 2: The second problem is that Meyer never denies that undirected causes can do some things. He in fact allows that natural processes can produce low levels of information. Thus, in one of his ID predictions he writes:

No undirected process will demonstrate the capacity to generate 500 bits of new information starting from a nonbiological source. (Signature, p. 496)

Likewise, when formulating his law of conservation of information, he notes that:

Invariably, evolutionary algorithms succeed in producing specified information (or its functional equivalent) as the result of preexisting information, or the programming skill of computer scientists, or both. With the exception of a small and quantifiable amount of information that may arise from the result of random effects, the information produced in these algorithms does not exceed the information that was provided to them by the programmers…” (Signature, p. 290)

Again, in formulating his law of conservation of information, Meyer notes expressly observe that over the entire history of the universe, it is possible that by chance 500 bits of information have arisen, “with 500 bits representing an upper bound for the entire observable universe.” (Signature, p. 294)

These three quotes show Meyer allows that undirected processes can produce low levels of specified information. So finding, as Jon Watts puts it, that “Biological information does arise without intelligent input” might not challenge Meyer’s thesis if it amounts to low levels of information. As we’ve seen, what Meyer wants to see more than 500 bits of new information arising by undirected processes. I'm sure that "fundamentally new genes and proteins" meeting that criteria would help a lot as well.

But as we also see in my article above, the Lenski experiment doesn’t demonstrate this.

Problem 3: Finally, Jon Watts and Nick Matzke both make a major mistake in characterizing Meyer’s “law of conservation of information”—and it’s the same mistake that Dennis Venema makes. All three of them ignore that Meyer’s law is quite explicitly formulated to apply only in the non-biological context, and he doesn’t claim his law applies after life arises. In a quote that directly refutes the comment from Watts and Matzke, Meyer writes:

Since I was not principally concerned with whether biological evolution could generate specified information, I decided to formulate a “conservative” conservation law—one that applied only to a nonbiological context (and thus not to any information-rich initial state). My statement of the law does not say anything about whether undirected natural processes could produce an increase in specified information starting with preexisting forms of life. But it does encapsulate what repeated experience had demonstrated about the flow of information starting from chemistry and physics alone.Here’s my version of the law of conservation of information: “In a nonbiological context, the amount of specified information initially present in a system, S, will generally equal or exceed the specified information content of the final system, Sf.” (Signature, p. 293)

In that quote above, Meyer’s is making it clear that in Signature in the Cell he is EXPLICITLY RESTRICTING HIS THESIS to the origin of the information in the first forms of life—information which had to have arisen in a non-biological context.

Unfortunately, many critics want to turn Meyer's thesis into something it isn't.

In fact, Venema’s quotes of Meyer’s discussion of Doug Axe’s work, mutation, and selection, come from an appendix at the end of the book that is not central to Meyer’s thesis. As I explained in my second article in this series, Meyer is looking at the origin of information in the first life, and “Meyer's primary point is that whatever evidence there may (or may not) be that natural selection can produce information is not relevant to the origin of information in the first life.” Meyer thus writes:

[M]any scientists recognized that Oparin's concept of prebiotic natural selection begged the question. Natural selection occurs only in organisms capable of reproducing or replicating themselves. Yet, in all extant cells, self-replication depends on functional and, therefore, sequence-specific DNA and protein molecules. As theoretical biologist Howard Pattee explains, "There is no evidence that hereditary evolution [natural selection] occurs except in cells which already have ... the DNA, the replicating and translating enzymes, and all the control systems and structures necessary to reproduce themselves." But this fact of molecular biology posed an obvious difficulty for Oparin's theory of prebiotic natural selection. In order to explain the origin of specified information in DNA, Oparin invoked a process that depends on preexisting sequence-specific (i.e. information-rich) DNA molecules. Yet the origin of these molecules is precisely what his theory needed to explain. As Christian de Duve explains, theories of prebiotic natural selection necessarily fail because they "need information which implies they have to presuppose what is to be explained in the first place."(Stephen C. Meyer, Signature in the Cell: DNA and the Evidence for Intelligent Design, pp. 274-275 (HarperOne, 2009) (emphasis in original).)

So Meyer’s “law of conservation of information” is explicitly formulated to apply only in a non-biological context. His book’s purpose is to explore that context, and not make strong claims outside of it. Venema, Matzke, and Watts like to quote Meyer’s one very brief foray outside of the non-biological context in an appendix. But given that biological evolution is not the subject of Meyer’s book (which rather investigates chemical evolution), this misrepresents Meyer’s central thesis.

Here’s my main point:

If Jon Watts is going to refute Meyer’s law of conservation of information, then he’s going to have to account for the fact that it was explicitly formulated to apply in a non-biological context—to the origin of information in the first life through non-biological processes. If Jon Watts wishes to cite experiments showing how biological information can arise through unguided chemical and physical processes, that’s great and it would meet Meyer’s thesis! But Jon Watts is not doing that. Like Venema, he’s citing examples from biological evolution via mutation and natural selection, which Meyer has quite compelling shown (see above quote) are irrelevant to the origin of information in the first life. Simply put, claiming that natura selection and random mutation can increase genetic information does not respond to Meyer's "law of conservation of information" as he has explicitly formulated it.

Thanks and I hope this helps show why so many critics are off-base in their rebuttals to Meyer.

Sincerely,

Casey

"There are many examples of increases in biomolecular information besides the LTEE"

I guess that settles it then. If you say so, it must be so. You don't have to give any examples. We'll just take your word for it.

Jon Watts | September 22, 2011 7:41 AM | Reply

Venema was responding to a specific claim that Meyer makes in Signature (and Dembski made a decade earlier) - namely the law of conservation of information. If ID is going to make claims in the form of a law - that information does not ever arise without direct intelligent input - then it is a sufficient, appropriate critique to show that one or more counterexamples exist. Biological information does arise without intelligent input, thus the law of conservation of information breaks down. There are many examples of increases in biomolecular information besides the LTEE.


That's the key point, Meyer's critics are all making it, and Casey Luskin's entire series of posts is devoted to obscuring and avoiding dealing with this critical issue.

If Meyer didn't want people raise the (numerous, extremely well-documented) cases of evolution creating new genes with new functions (something which even Behe accepts), and thus creating new information, he shouldn't have proposed a "law of conservation of information" and then based his entire book upon that argument.

Everyone go search on "origin of new genes" on Google Scholar to see what actual scientists have published on this topic.

Luskin's only response to this work has been a post that claims that inferring gene duplication, point mutations, and natural selection to explain the sequence and diversity features we see when examining e.g. a series of gene sequences that are obviously copies of each other with more or less modified sequences has been to call the invocation of these these well-known, well-documented processes no better than "waving a magic wand". No, Casey: it's your side that invokes magic to explain new genes. Your explanation is: no gene --> poof, a miracle occurs --> new gene.

Hello Casey. I have question. The Behe paper reports some cases of adaptive gain of funcional coded elements resulting from mutations.
Are those instances an increase of Functionally complex specified information resulting from mutations?

How sad for a Christian at a Christian University to be importing gnostic philosophy into the science classroom. Aren't there any theological checks and balances at the School?

Great job Casey. You have some amazing skills to digest and organize information. I'm repeatedly amazed at the tepid arguments of BioLogos folks and how easy it is to dismantle them with readily available data. Thanks for showing the way!

Venema was responding to a specific claim that Meyer makes in Signature (and Dembski made a decade earlier) - namely the law of conservation of information. If ID is going to make claims in the form of a law - that information does not ever arise without direct intelligent input - then it is a sufficient, appropriate critique to show that one or more counterexamples exist. Biological information does arise without intelligent input, thus the law of conservation of information breaks down. There are many examples of increases in biomolecular information besides the LTEE.

Naturalism may have seemed to be the more "scientific" stance when faced with the alternatives. But as soon as one tries to defend the naturalist belief, blatant compromise of this "scientific" principle is inevitable.
If anything, are we not witnessing the very slow and gradual demise of this race of e-coli? This is almost the opposite of Darwinian evolution.
Yet the naturalist must obey his religious convictions and compromise his "scientific" principle by believing that the e-coli is ^evolving^.

On Don Quixote

“He has become obsessed with books of chivalry, and believes their every word to be true, despite the fact that many of the events in them are clearly impossible.” - wiki

I think the difficulty arises in the debate because of the “Quixote” element. The belief that Darwin’s Theory somehow saves mankind from superstition is fundamental to the resistance being displayed and to defend it, in the New Atheist mind, is a heroic endeavour. All genuine Scientists are somehow duty bound to defend Natural selection acting on random variation.

When theories arise that threaten our world view and attack our individual vision of how the Universe is suppose to be, we are galvanized to take action and in this case spend hours of research time debunking the opposing arguments. We saw this in the “Black Hole Wars” and in the “Big Bang” conflagration with Fred Hoyle.

Windmills are just so; and so are theories. But how easily are those windmills turned into giants when a perceived threat arises. And Don Quixote rides out, tours America, writes books and critiques others perceptions; doing so whilst oblivious to the arguments presented in rebuttal. This issue is really not about science.

An informative analysis, keep up the good work.

Twenty years ago while writing PCB auto routing software I designed an evolutionary algorithm that
connected sets of pins. It could connected most everything but some patterns would fail no matter how long it ran.

Analysis of structures the algorithm couldn't route revealed constraining bias that prevented the process from converging and to fix it the software would have to recognize it was stuck and bias randomness to compensate for it.

It may be possible to formalize and prove evolutionary process in general have limits, similar to how the busy beaver proved certain state machine outcomes are un-computable.


1. The Modern Synthesis is dead. (MacNeill - The Evolution List)

2. The Tree of Life is being politely buried. (Bapteste et al)

3. There is search for an extended synthesis.(Massimo Pigliucci)

4. Life is information technology and information cannot pass the Cybernetic Cut. (D. Abel)

5. Paradigm cases of semantic information are the products of Intelligent Agents ( The Stanford Encyclopedia of Philosphy - Biological Information)


We are getting there.

A quote from the paper that Luskin misses: “If the phenotype of the Lenski Cit strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.”

See the word “IF”? Behe doesn’t know what class it falls in. He’s listing the possibilities. ALL THE POSSIBILITES, including “a noteworthy gain-of-FCT mutation.” Considering the review gives many examples of gain-of-FCT mutations, it is wholly disingenuous to conclude Lenski’s must be loss of function/information, and that gain of function/information are impossible.