Tag Archives: Mutation

Peer-reviewed paper: Michael Behe’s “First Rule of Adaptive Evolution”

Apologetics and the progress of science
Apologetics and the progress of science

JoeCoder was writing some JavaScript code last night and he ran into a problem where a 3rd-party open source library was not performing as expected. So he got the non-minified version of the library and commented out two lines to get the behavior he wanted. He said this to me “Michael Behe’s first rule of adaptive evolution has been confirmed once again.” So, let’s take a look at Mike Behe’s first rule of adaptive evolution.

The paper was published in the Quarterly Review of Biology. I found it on PubMed.


Adaptive evolution can cause a species to gain, lose, or modify a function; therefore, it is of basic interest to determine whether any of these modes dominates the evolutionary process under particular circumstances. Because mutation occurs at the molecular level, it is necessary to examine the molecular changes produced by the underlying mutation in order to assess whether a given adaptation is best considered as a gain, loss, or modification of function. Although that was once impossible, the advance of molecular biology in the past half century has made it feasible. In this paper, I review molecular changes underlying some adaptations, with a particular emphasis on evolutionary experiments with microbes conducted over the past four decades. I show that by far the most common adaptive changes seen in those examples are due to the loss or modification of a pre-existing molecular function, and I discuss the possible reasons for the prominence of such mutations.

By far the most common adaptive changes in the examples we have are due to loss of function or modification of pre-existing function?

Evolution News has a post up about the paper.


After reviewing the effects of mutations upon Functional Coding ElemenTs (FCTs), Michael Behe’s recent review article in Quarterly Review of Biology, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” offers some conclusions. In particular, as the title suggests, Behe introduces a rule of thumb he calls the “The First Rule of Adaptive Evolution”: “Break or blunt any functional coded element whose loss would yield a net fitness gain.” In essence, what Behe means is that mutations that cause loss-of-FCT are going to be far more likely and thus far more common than those which gain a functional coding element. In fact, he writes: “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.” Since organisms will tend to evolve along the most likely pathway, they will tend to break or lose an FCT before gaining a new one. He explains:

It is called the “first” rule because the rate of mutations that diminish the function of a feature is expected to be much higher than the rate of appearance of a new feature, so adaptive loss-of-FCT or modification-of-function mutations that decrease activity are expected to appear first, by far, in a population under selective pressure.(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 argues that this point is empirically supported by the research reviews in the paper. He writes:

As seen in Tables 2 through 4, the large majority of experimental adaptive mutations are loss-of-FCT or modification-of-function mutations. In fact, leaving out those experiments with viruses in which specific genetic elements were intentionally deleted and then restored by subsequent evolution, only two gain-of-FCT events have been reported

After asking “Why is this the case?” Behe states, “One important factor is undoubtedly that the rate of appearance of loss-of-FCT mutations is much greater than the rate of construction of new functional coded elements.” He draws sound and defensible conclusions from the observed data:

Leaving aside gain-of-FCT for the moment, the work reviewed here shows that organisms do indeed adapt quickly in the laboratory–by loss-of-FCT and modification-of-function mutations. If such adaptive mutations also arrive first in the wild, as they of course would be expected to, then those will also be the kinds of mutations that are first available to selection in nature. … In general, if a sequence of genomic DNA is initially only one nucleotide removed from coding for an adaptive functional element, then a single simple point mutation could yield a gain-of-FCT. As seen in Table 5, several laboratory studies have achieved thousand to million-fold saturations of their test organisms with point mutations, and most of the studies reviewed here have at least single-fold saturation. Thus, one would expect to have observed simple gain-of-FCT adaptive mutations that had sufficient selective value to outcompete more numerous loss-of- FCT or modification-of-function mutations in most experimental evolutionary studies, if they had indeed been available.

But this stark lack of examples of gain-of-functional coding elements can have important implications:

A tentative conclusion suggested by these results is that the complex genetic systems that are cells will often be able to adapt to selective pressure by effectively removing or diminishing one or more of their many functional coded elements.

Behe doesn’t claim that gain-of-function mutations will never occur, but the clear implication is that neo-Darwinists cannot forever rely on examples of loss or modification-of-FCT mutations to explain molecular evolution. At some point, there must be gain of function.

Now, there was a response to this paper from Jerry Coyne on his blog, and then a rebuttal from Mike Behe in a separate article on Evolution News.

Convergence detected in the genetic structure of bats and dolphins

Apologetics and the progress of science
Apologetics and the progress of science

We have to start this post with the definition of convergence in biology.

In evolutionary biology, convergent evolution is the process whereby organisms not closely related (not monophyletic), independently evolve similar traits as a result of having to adapt to similar environments or ecological niches.

It is the opposite of divergent evolution, where related species evolve different traits.

On a molecular level, this can happen due to random mutation unrelated to adaptive changes; see long branch attraction. In cultural evolution, convergent evolution is the development of similar cultural adaptations to similar environmental conditions by different peoples with different ancestral cultures. An example of convergent evolution is the similar nature of the flight/wings of insects, birds, pterosaurs, and bats.

All four serve the same function and are similar in structure, but each evolved independently.

Jonathan Wells explains the problem that convergence poses for naturalistic evolution:

Human designers reuse designs that work well. Life forms also reuse certain structures (the camera eye, for example, appears in humans and octopuses). How well does this evidence support Darwinian evolution? Does it support intelligent design more strongly?

Evolutionary biologists attribute similar biological structures to either common descent or convergence. Structures are said to result from convergence if they evolved independently from distinct lines of organisms. Darwinian explanations of convergence strain credulity because they must account for how trial-and-error tinkering (natural selection acting on random variations) could produce strikingly similar structures in widely different organisms and environments. It’s one thing for evolution to explain similarity by common descent—the same structure is then just carried along in different lineages. It’s another to explain it as the result of blind tinkering that happened to hit on the same structure multiple times. Design proponents attribute such similar structures to common design (just as an engineer may use the same parts in different machines). If human designers frequently reuse successful designs, the designer of nature can surely do the same.

I’m a software engineer, and we re-use components all the time for different programs that have no “common ancestor”. E.g. – I can develop my String function library and use it in my web application and my Eclipse IDE plug-in, and those two Java programs have nothing in common. So you find the same bits in two different programs because I am the developer of both programs. But the two programs don’t extend from a common program that was used for some other purpose – they have no “common ancestor” program.

Now with that in mind, take a look at this recent article from Science Daily, which Mysterious Micah sent me.


The evolution of similar traits in different species, a process known as convergent evolution, is widespread not only at the physical level, but also at the genetic level, according to new research led by scientists at Queen Mary University of London and published in Nature this week.

The scientists investigated the genomic basis for echolocation, one of the most well-known examples of convergent evolution to examine the frequency of the process at a genomic level.

Echolocation is a complex physical trait that involves the production, reception and auditory processing of ultrasonic pulses for detecting unseen obstacles or tracking down prey, and has evolved separately in different groups of bats and cetaceans (including dolphins).

The scientists carried out one of the largest genome-wide surveys of its type to discover the extent to which convergent evolution of a physical feature involves the same genes.

They compared genomic sequences of 22 mammals, including the genomes of bats and dolphins, which independently evolved echolocation, and found genetic signatures consistent with convergence in nearly 200 different genomic regions concentrated in several ‘hearing genes’.

[…]Consistent with an involvement in echolocation, signs of convergence among bats and the bottlenose dolphin were seen in many genes previously implicated in hearing or deafness.

“We had expected to find identical changes in maybe a dozen or so genes but to see nearly 200 is incredible,” explains Dr Joe Parker, from Queen Mary’s School of Biological and Chemical Sciences and first author on the paper.

“We know natural selection is a potent driver of gene sequence evolution, but identifying so many examples where it produces nearly identical results in the genetic sequences of totally unrelated animals is astonishing.”

Nature is the most prestigious peer-reviewed science journal. This is solid material.

There is an earlier article from 2010 in New Scientist that talked about one of the previous genes that matched for hearing capability.


Bats and dolphins trod an identical genetic path to evolve a vital component of the complex sonar systems they use to pursue and catch prey.

The finding is unusual, because although many creatures have independently evolved characteristics such as eyes, tusks or wings, they usually took diverse genetic routes to get there.

Analysis of a specific gene has now demonstrated that although bats live in air and dolphins in water, where sound travels five times faster, they independently evolved a near-identical gene that allows them to accept high-frequency sound in the ear – vital for sonar.

The gene makes prestin, a protein in hair cells of the cochlea, which is the organ in the inner ear where sonar signals are accepted and amplified. Prestin changes shape when exposed to high-frequency sound, and this in turn deforms the fine hair cells, setting off an electrical impulse to the brain. So the protein has the important jobs of detecting and selecting high-frequency sounds for amplification.

When researchers examined the molecular structure of the prestin gene from a range of animals, they found that the variants in echolocating bats and dolphins were virtually indistinguishable.

Indistinguishable genes in animals that don’t share a common ancestor? Maybe a better explanation for the evidence we have is – common designer.

John C. Sanford’s genetic entropy hypothesis

Apologetics and the progress of science
Apologetics and the progress of science

JoeCoder sent me a recent peer-reviewed paper by John C. Sanford, so I’ve been trying to find something written by him at a layman’s level so I could understand what he is talking about. (I am just a software engineer, not an expert in genetics). His CV is posted at the Cornell University web page.

I found this 20-minute video of an interview with him, in which he explains his thesis:

The most important part of that video is Sanford’s assertion that natural selection cannot remove deleterious mutations from a population faster than they arrive.

And I also found a review of a book that he wrote that explains his ideas at the layman level.

It says:

Dr. John Sanford is a plant geneticist and inventor who conducted research at Cornell University for more than 25 years. He is best known for significant contributions to the field of transgenic crops, including the invention of the biolistic process (“gene gun”).

[…]Sanford argues that, based upon modern scientific evidence and the calculations of population geneticists (who are almost exclusively evolutionists), mutations are occurring at an alarmingly high rate in our genome and that the vast majority of all mutations are either harmful or “nearly-neutral” (meaning a loss for the organism or having no discernible fitness gain). Importantly, Sanford also establishes the extreme rarity of any type of beneficial mutations in comparison with harmful or “nearly-neutral” mutations. Indeed, “beneficial” mutations are so exceedingly rare as to not contribute in any meaningful way. [NOTE: “Beneficial” mutations do not necessarily result from a gain in information, but instead, these changes predominantly involve a net loss of function to the organism, which is also not helpful to [Darwinism]; see Behe, 2010, pp. 419-445.] Sanford concludes that the frequency and generally harmful or neutral nature of mutations prevents them from being useful to any scheme of random evolution.

[…]In the next section of the book, Sanford examines natural selection and asks whether “nature” can “select” in favor of the exceedingly rare “beneficial” mutations and against the deleterious mutations. The concept of natural selection is generally that the organisms that are best adapted to their environment will survive and reproduce, while the less fit will not. Sanford points out that this may be the case with some organisms, but more commonly, selection involves chance and luck. But could this process select against harmful mutations and allow less harmful or even beneficial mutations to thrive? According to Sanford, there are significant challenges to this notion.

Stanford is a co-author of an academic book on these issues that has Dembski and Behe as co-authors.

Now, I do have to post something more complicated about this, which you can skip – it’s an abstract of a paper he co-authored from that book:

Most deleterious mutations have very slight effects on total fitness, and it has become clear that below a certain fitness effect threshold, such low-impact mutations fail to respond to natural selection. The existence of such a selection threshold suggests that many low-impact deleterious mutations should accumulate continuously, resulting in relentless erosion of genetic information. In this paper, we use numerical simulation to examine this problem of selection threshold.

The objective of this research was to investigate the effect of various biological factors individually and jointly on mutation accumulation in a model human population. For this purpose, we used a recently-developed, biologically-realistic numerical simulation program, Mendel’s Accountant. This program introduces new mutations into the population every generation and tracks each mutation through the processes of recombination, gamete formation, mating, and transmission to the new offspring. This method tracks which individuals survive to reproduce after selection, and records the transmission of each surviving mutation every generation. This allows a detailed mechanistic accounting of each mutation that enters and leaves the population over the course of many generations. We term this type of analysis genetic accounting.

Across all reasonable parameters settings, we observed that high impact mutations were selected away with very high efficiency, while very low impact mutations accumulated just as if there was no selection operating. There was always a large transitional zone, wherein mutations with intermediate fitness effects accumulated continuously, but at a lower rate than would occur in the absence of selection. To characterize the accumulation of mutations of different fitness effect we developed a new statistic, selection threshold (STd), which is an empirically determined value for a given population. A population’s selection threshold is defined as that fitness effect wherein deleterious mutations are accumulating at exactly half the rate expected in the absence of selection. This threshold is mid-way between entirely selectable, and entirely unselectable, mutation effects.

Our investigations reveal that under a very wide range of parameter values, selection thresholds for deleterious mutations are surprisingly high. Our analyses of the selection threshold problem indicate that given even modest levels of noise affecting either the genotype-phenotype relationship or the genotypic fitness-survival-reproduction relationship, accumulation of low-impact mutations continually degrades fitness, and this degradation is far more serious than has been previously acknowledged. Simulations based on recently published values for mutation rate and effect-distribution in humans show a steady decline in fitness that is not even halted by extremely intense selection pressure (12 offspring per female, 10 selectively removed). Indeed, we find that under most realistic circumstances, the large majority of harmful mutations are essentially unaffected by natural selection and continue to accumulate unhindered. This finding has major theoretical implications and raises the question, “What mechanism can preserve the many low-impact nucleotide positions that constitute most of the information within a genome?”

If you think all this is interesting, there is a much longer lecture here, which I have not watched. JoeCoder has watched it and he endorses it.

Now I have been told by JoeCoder that there are many critical responses to his hypothesis, most of which have to do with whether natural selection can overcome the difficulty he is laying out. But since this is not my area of expertise, there is not much I can say to adjudicate here, I won’t be able to respond to these. I hope that I will have time to come back to this and read about it at some point. I do have an e-book of the that collection of papers book I linked to above.

Positive arguments for Christian theism

New study: natural selection can act to impede speciation

Australian Walking Stick
Australian Walking Stick

My friend KL sent me this press release from the University of Colorado at Boulder.

It says:

An intriguing study involving walking stick insects led by the University of Sheffield in England and the University of Colorado Boulder shows how natural selection, the engine of evolution, can also impede the formation of new species.

The team studied a plant-eating stick insect species from California called Timema cristinae known for its cryptic camouflage that allows it to hide from hungry birds, said CU-Boulder Assistant Professor Samuel Flaxman. T. cristinae comes in several different types — one is green and blends in with the broad green leaves of a particular shrub species, while a second green variant sports a white, vertical stripe that helps disguise it on a different species of shrub with narrow, needle-like leaves.

While Darwinian natural selection has begun pushing the two green forms of walking sticks down separate paths that could lead to the formation of two new species, the team found that a third melanistic, or brown variation of T. cristinae appears to be thwarting the process, said Flaxman. The brown version is known to successfully camouflage itself among the stems of both shrub species inhabited by its green brethren, he said.

Using field investigations, laboratory genetics, modern genome sequencing and computer simulations, the team concluded the brown version of T. cristinae is shuttling enough genes between the green stick insects living on different shrubs to prevent strong divergent adaptation and speciation. The brown variant of the walking stick species also is favored by natural selection because it has a slight advantage in mate selection and a stronger resistance to fungal infections than its green counterparts.

“This is one of the best demonstrations we know of regarding the counteractive effects of natural selection on speciation,” said Flaxman of CU-Boulder’s Department of Ecology and Evolutionary Biology, second author on the new study. “We show how the brown population essentially carries genes back and forth between the green populations, acting as a genetic bridge that causes a slowdown in divergence.”

A paper on the subject appeared in a recent issue of the journal Current Biology. 

[…]“This movement of genes between environments slows down the genetic divergence of these stick insect populations, impeding the formation of new species,” said Aaron Comeault, a former CU-Boulder graduate student and lead study author who conducted the research while at the University of Sheffield.

So, in the past I had read that natural selection can act as a stabilizing force in nature – keeping the organism operating within a type. This study seems to be confirmation of that. But there are other problems with generating macro-evolutionary change.

Also related to the problem raised by the study is this problem of genetic drift, which also works against the preservation of beneficial mutations.

Evolution News explains the genetic drift problem:

Evolutionary biologists often assume that once mutations produce a functionally advantageous trait, it will easily spread (become “fixed”) throughout a population by natural selection. For example, imagine a population of brown-haired foxes that lives in a snowy region. One fox is born with a mutation that turns its fur coat white, rather than brown. This fox now has an advantage in hunting prey and escaping predators, because its white fur provides it with camouflage. The white fox survives, passing its genes on to its offspring, which are also adept at surviving and reproducing. Over time, the white-haired trait spreads throughout the population.

This is how it’s supposed to work — in theory. In the real world, however, merely generating a functionally advantageous trait does not guarantee it will persist, or become fixed. For example, what if by chance the white fox trips, breaks a leg, and gets eaten by a predator — never passing on its genes? Random forces or events can prevent a trait from spreading through a population, even if it provides an advantage. These random forces are lumped together under the name “genetic drift.” When biologists run the mathematics of natural selection, they find that unless a trait gives an extremely strong selective advantage, genetic drift will tend to overwhelm the force of selection and prevent adaptations from gaining a foothold in a population.

This underappreciated problem has been recognized by some evolutionary scientists who are skeptical of the ability of natural selection to drive the evolutionary process. One of those scientists is Michael Lynch, an evolutionary biologist at Indiana University, who writes that “random genetic drift can impose a strong barrier to the advancement of molecular refinements by adaptive processes.”2 He notes that the effect of drift is “encouraging the fixation of mildly deleterious mutations and discouraging the promotion of beneficial mutations.”3

I guess the point of this is that if someone wants to convince you that macro-evolution is possible through the mechanisms of random mutation and natural selection, then they have some work to do. And it’s more work than just asserting that it happened.

People who are technical may benefit from reading Michael Behe’s book “The Edge of Evolution”, which studies how likely it is to get several positive adaptations in a row within a reasonable period of time.

UPDATE: A biologist friend tells me that “whether natural selection is driving speciation or preventing it, in neither case is it explaining how these organisms came to be in the first place. It only explains how existing organisms interact with their environment. And this can be explained at least as well through intelligent design as through naturalistic processes.” She also says that natural selection can drive speciation, but still within a kind.

Three logical prerequisites for biological evolution to work

Biologist, blogger and super-mom Lindsay has written a post that explains what supporters of Darwinian mechanisms have to prove in order to explain the origin and diversity of life.

Here are the three things that Darwinists must demonstrate:

  1. It is possible to add biological information.
  2. There are more upward steps than downward steps (or at least a way to get more upward steps than downward steps at least some of the time).
  3. There does exist a gradual genetic pathway that can be climbed in tiny, incremental steps.

So first of all, the main two arguments for intelligent design and against naturalism are the origin of life and the Cambrian explosion. Both involve massive infusions of new biological information. So Lindsay is right to focus on whether Darwinism can add new biological information. But I wanted to focus on number three, because I really think that her post is about the burden of proof on Darwinists more than it is about our burden of proof. And we do need to get used to asking Darwinists for the evidence for their view.

Take a look at the detail on number three:

In order for evolution to be true, not only does information have to be added over time, but each successive change must occur in a living organism and it must be conserved by being passed on to offspring. Thus, the change cannot kill the organism or seriously disable it, or the change will not be passed on. This must be the case for EVERY step in the entire evolutionary sequence, no matter how small. At every step you must have a functional organism. Thus, the changes must be gradual enough that the tiny upward steps (if they exist) can achieve each new level without killing or disabling the organism. To use a simplistic analogy, if one tries to change from one word to another by changing one letter at a time (cat to cot to dot to dog, for example), there must, at every step, be an actual word that can be reached by changing one letter. In the Mount Improbable analogy, this means that there can be no upward jumps in the trail. If the maximum possible upward step is 6 inches, then there can be no 6 foot cliffs along the trail, or even 7 inch steps. If ever there is a step which requires more information than unguided evolution can provide, then evolution is falsified in that instance. It cannot account for the change in information if that is the case.

Now I have never seen a gradual genetic pathway from one body plan to another in any peer-reviewed paper. I am talking about from one phyla to another. What I need to see to believe in the ability of Darwinian mechanisms to drive change from one body plan to another is that sequence of changes at the genetic level. And I don’t just need to see the steps, I need to see the probabilities of getting the correct sequence of changes at the genetic level within the time available by chance. That’s what Darwinists assert in their theory – that’s what they need to prove. Talking about how one creature looks like another creature is irrelevant. My car looks like my Dads car, because we drive the same model, but different model years – and both cars are designed.

When people ask our side for evidence for our claims, we are able to produce the evidence to substantiate our claims, e.g. – cosmic fine-tuning factors or protein sequencing probabilities. I would like to see the other side do the same, and not just tell me a story.

If you are looking to understand what the other side has to prove, and in a concise way, read her post.