Biological Information and Intelligent Design: evolving new protein folds

The details are all there in the paper from 1984 that I cited. Feel free to have a look.

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Thanks Dennis :slight_smile:

No problem. :slight_smile:

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Isn’t evolutionary life wonderful?

Science has done a good job determining how life forms change. It has not done such as good job exploring why they change.

Hi Steve
Thanks for the paper. This is a fascinating case study.

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You’re welcome. I think that paper was groundbreaking because it showed how prokaryotes can “invent” new genes without the benefit of extra DNA. The phenomenon is now called “overprinting” and involves frame shifts as Ohno found in 1984. According to this recent paper, we now have four known examples of this. Overprinting shows how easy it is (in principle) for new genetic information to arise through small changes, even in environments like bacterial genomes where there is almost no unused genetic material sitting around.

Most eukaryotes, and basically all animals, have gigantic amounts of non-coding DNA from which to accidentally discover new coding sequences. So we animals have many more opportunities to create a new domain or an entirely new gene overnight. I admit I used to think that this was probably pretty rare. But I think I was wrong; see some of these recent open access papers:

New genes from non-coding sequence: the role of de novo protein-coding genes in eukaryotic evolutionary innovation

Origins of De Novo Genes in Human and Chimpanzee

The Recent De Novo Origin of Protein C-Termini

Disclosure: a kid of mine is a grad student in the Masel lab, which published the last paper.

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Sir, I’ve been fascinated by the nylonase topic for some time, but continue to find disagreement when I search the web about whether this is a de novo protein or an adaptation of something pre-existent.

Searching through various articles, I found a study of what I’m guessing must be the 392 amino acid length enzyme you refer to here - in a JMB article “(Nylon-oligomer Degrading Enzyme/Substrate Complex: Catalytic Mechanism of 6-Aminohexanoate-dimer Hydrolase”) I found the following:

“Recently, we identified the three-dimensional structure of the Hyb-24 (an EII/EII′ hybrid containing five amino acid replacements… in the EII′ protein… The fold adopted by the 392 amino acid residue polypeptide generated a two-domain structure… In contrast to the strict recognition of the amide substrates, the enzyme hydrolyzes various carboxylesters with different acyl chains. Based on these findings, we have proposed that amino acid replacements in the catalytic cleft of a pre-existing esterase with the β-lactamase-fold resulted in the evolution of the nylon oligomer hydrolase… In addition, we discuss how the hydrolytic activities toward nylon oligomer emerged in the catalytic cleft of an esterase with the β-lactamase fold, while retaining the original esterolytic function.”

I’m not familiar with the literature, so I may be misreading it; but so far as I can follow, they seem to be speaking about the same nylon-digesting 392-amino acid length enzyme you mention, but seem to believe it to have resulted from specific amino acid replacements from a pre-existing esterase. Can you clarify?

Hi Daniel - thanks for the question.

The “pre-existing esterase” is the one that arose from the frameshift. It then duplicates, and the duplicate undergoes the amino acid substitutions (which make it a much better nylonase than the initial one). So, the end nylonase is the result of a string of events. The paper you cite is looking at the duplicate / substitutions.


Hi Dennis:

The nylonase example does not support evolution very well. In fact, it is problematic. A good general rule of thumb to keep in mind is that we need to be very careful in describing any “new” gene arising in a modern biological cell as an instance of evolution and evidence that therefore proteins can evolve. Nylonase is a good example of this. It is a case of directed adaptation–a repeatable process, rather than a result of blind, random mutations. Rather than serving as an example of evolution, nylonase, as with other such cases, raises the problem of how evolution could create adaptation mechanisms for future, unforeseen, environmental challenges. Such mechanisms would not provide any fitness improvement (without resorting to extreme just-so stories).

You’re eliding a major point: selection acts on heritable variation. Only a teeny-tiny amount of that variation is new mutations. The vast majority of variation already exists.

I realize that pretending that existing variation doesn’t exist makes for better polemics, though…


Welcome back to your Home Away from Home, @Cornelius_Hunter!

There is a kind of Vanilla sameness to your objections to the various biological minutia presented in support of God-guided Evolution. It usually contains, in one form or another, “how could Evolution anticipate that?”

But is this really fair? Isn’t this category of objection really more suited to disputes with Atheists (and even more obscure groups who are not Atheists but don’t think God is involved in Natural Selection)?

Intelligent Design of your kind really faces quite an obstacle. You want to say that because some things work out so amazingly well at the biological or molecular level, it demonstrates the Intentions of a Great Designer.

Many BioLogos supporters, such as myself, can find moments like this too… and see our belief in God-Guided evolution as sustained.

But then the difference appears on the horizon, bearing down at both camps:

The natural world shows lots of cases where it seems there has been well-planned intention … And the natural world is full of cases where it would seem only unintentional bungling seems to be at work … not so much because of a mistake, but because of a Lack of appearance of intelligence, planning or anticipation.

For example, look at the Vitamin C issue in the exhibit below. The God-Guided-Evolutionary model would predict that whenever we find an animal without a functioning Vitamin C gene… if that animal is not a primate, then the faulty Vitamin C genetics is almost certainly corrupted in a way different from the genetic corruption in the Primate lineages.

Cornelius, how can you play both sides of the street, unless you are more or less a BioLogos-type endorsing Intelligent Design? In a sense, BioLogos occupies the “sweet spot” of the evolutionary dilemma. We can look to God when we see something amazing - - virtually miraculous… and yet we can still see the un-intentioned clunkiness of a process that has taken millions of years to arrive at its current state!

Hi Cornelius, and welcome back to BioLogos.

Are you saying the frameshift mutation that produced the original nylonase was intentionally engineered by the bacterium in which it occurred? What is your evidence for that claim?

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Are you saying that the bacteria’s need to digest nylon was a foreseen challenge? And if so, what could possibly qualify as a future unforeseen challenge?

How do you tell the difference between a ‘directed adaptation’ and ‘blind mutation?’ The above posts clearly described multiple mutations which occurred in the history of the nylonase. Are you just assuming that they must have been ‘directed?’ Why?

And how does that make it problematic evidence for evolution?

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Sure, there is plenty of evidence. I’ll list some of it:

  1. Directed adaptation is a fact (though evolutionists resist these findings and their implications).

  2. Nylon metabolism arises very rapidly, and is repeatable. We see this over and over in directed adaptation mechanisms, and it falsifies evolutionary expectations.

  3. Researchers hypothesize that nylon metabolism is a stress response, which makes perfect sense, not chance evolution.

  4. De novo evolution of functional proteins by chance is astronomically unlikely. This is very basic, and is well understood from several angles, including theoretical and experimental.

Ohno’s 1984 frameshift hypothesis has not stood the test of time very well, but even if it was true, what that would indicate is that there is something very special about that sequence, not that, what-do-you-know, we’ve stumbled upon an example of chance evolution of proteins, arising in an evolutionary nanosecond. This is just another example of bad science, and nylonase seems to qualify as another icon of evolution.

Rather than reckoning with the science, and accurately perceiving that nylon metabolism is telling us something interesting about the cell’s adaptation capabilities, evolutionists have erroneously force-fit the evidence into their chance narrative, and claimed victory. Here’s an example of this which you may recognize:

Put another way, if only one in 10 to the 77th proteins are functional, there should be no way that this sort of thing could happen in billions and billions of years, let alone 40. Either this was a stupendous fluke (and stupendous isn’t nearly strong enough of a word), or evolution is in fact capable of generating the information required to form new protein folds. And if this can happen in 40 years, what might millions of years of evolution produce?

This is just all backwards. The problem is that evolutionary thinking does not allow us to engage with the obvious explanation: directed adaptation. So instead we dispense with well-established science.

Yes, this is what it is all about–those “bungles and errors” as Ray and Cudworth put it.

Here’s a thought—if God directed those particular bacteria to produce nylonase against such enormous odds and in an environment of evolutionary thinking which would not allow anyone to engage with alternative explanations, the only obvious conclusion is that God wants us to believe in evolution.

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Hello Dr. Hunter,

Welcome back! I hope all is going well for you, your family and your students.

I think that your summary of the Prijambada, et al.'s paper left out some important details. The researchers state:

a molecular basis for the emergence of nylon oligomer metabolism in PAO5502 is still unknown

Thus it would seem premature to draw conclusions one way or another regarding the mechanisms behind the adaptation they observed. However, they do note that earlier research by Lenski and Mittler shows that the mutation rate in bacterial genomes can increase in response to environmental stress:

Recently, it was reported that simple polymerase errors increase in the adaptive mutation from Lac2 to Lac1 in E. coli (2, 17) and that molecular mechanisms by which adaptive mutation occurs include recombination (4). Lenski and Mittler have observed a 10,000-fold increase in Mu element excision due to starvation (10).

Applying Lenski and Mittler’s conclusions to their experimental observations, Prijambada, et al. make this conjecture:

Since the nylon oligomer has no detectable toxicity toward microorganisms, the wild-type cells could be maintained in a starved condition for a long period. After the cells accumulated the required genetic alteration to make a cryptic region active, cells grew in the nylon oligomer medium. The high frequency (10^-3) of the hypergrowing mutants of parental strain PAO1 on medium containing Ahx might be a result of a high mutation rate under the condition of starvation.

Nothing about Prijambada’s paper would seem to challenge the consensus regarding genetic mutation and variation as the source of biological adaptation. Of course, their finding could mess up some molecular clock calculations! :grinning: At the same time, the notion that mutation rates can accelerate under some circumstances is already comfortably a part of the emerging evolutionary synthesis.*

However, you and I can say by faith that our Creator designed all of life marvelously. The genetic mechanisms He envisioned at the time of the Big Bang are well-suited to life on our planet, including some baked-in capabilities to increase mutation rates at the right times. If that’s what you mean by directed adaptation, I am in full agreement.


Chris Falter

*Since I am not a biologist, my understanding of the EES is based on popular reporting. I would welcome any feedback/corrections from real biologists such as yourself. Thanks!


Your one-liner was pretty much non-responsive to my question. Let me re-phrase it:

So you don’t think it is a strange coincidence that all primates who could share a common ancestor have a defective Vitamin C gene that are defective in the very same way … rather than having differently defective Vitamin C genes, like the Guinea Pig and the Fruit Bat has?

Why would God seem so determined to make it look like Evolultion did occur in the Primate “kind”?

In fact, I would interpret this as God trying to convince you that Primate Evolution did occur!


That is a very good point. It looks so very much like evolution occurred, so why not believe it did? Sure, if evolution didn’t happen, it makes God look like a magician who is out to fool us. But if he’s really out to fool us, we should just go along with it. After all, no movie maker or theme park attraction designer would ever want to hear that his special effects look fake. Movies, etc. are supposed to fool us; they draw us into the story and make us forget reality for a bit.