We all know the neo-Darwinian story: random mutations are naturally selected for fitness, leading to innovation over time. By this elegant process, bacteria over billions of years became humans. But when you eliminate the question-begging circular arguments, distracting definitions, and ideological assumptions, can evolutionists really demonstrate any unambiguous cases of innovation? To clear away clutter, here’s what we mean by eliminating faulty answers:
- Question-begging circular arguments: This is the assumption that anything that survives must be fit, because only the fittest survive. Tom Bethell discusses this tautological formulation of evolution in Darwin’s House of Cards.
- Distracting definitions: Words like fitness, positive selection, and beneficial mutation collapse into circularity when there is no measure for them except survival.
- Ideological assumptions: This is the prevention of debate by defining science as methodological naturalism, thus ruling out design. Evolutionary innovation then becomes a deduction, not on observation: if some adaptive structure exists, it must have evolved. Bethell also discusses this.
Two classic cases of innovation claimed by evolutionists are the citrate story in Lenski’s lab and the nylonase story. For the example of citrate metabolism, Michael Behe explained that it was a switch-on of a pre-existing function, not an innovation. Ditto for the nylonase story, which Ann Gauger recently revisited. Now, let’s look into some recent papers for more examples of innovation by chance mutations. The papers promise them; do they deliver?
What better place to start than a paper edited by Richard Lenski himself? Let’s search for innovation in their paper in PNAS, “Hitchhiking and epistasis give rise to cohort dynamics in adapting populations.” The opening sentence sounds promising: “Beneficial mutations are the driving force of adaptive evolution.” Indeed, this paper is full of the words beneficial mutations, adaptive, and fitness. Sounds like a good place to hunt, as we watch them tweak yeast genes to see if something novel, something innovative, arises by random chance. They will even consider mutations that might work in synergy to provide a new benefit. Here’s the Abstract:
Beneficial mutations are the driving force of adaptive evolution. In asexual populations, the identification of beneficial alleles is confounded by the presence of genetically linked hitchhiker mutations. Parallel evolution experiments enable the recognition of common targets of selection; yet these targets are inherently enriched for genes of large target size and mutations of large effect. A comprehensive study of individual mutations is necessary to create a realistic picture of the evolutionarily significant spectrum of beneficial mutations. Here we use a bulk-segregant approach to identify the beneficial mutations across 11 lineages of experimentally evolved yeast populations. We report that nearly 80% of detected mutations have no discernible effects on fitness and less than 1% are deleterious. We determine the distribution of driver and hitchhiker mutations in 31 mutational cohorts, groups of mutations that arise synchronously from low frequency and track tightly with one another. Surprisingly, we find that one-third of cohorts lack identifiable driver mutations. In addition, we identify intracohort synergistic epistasis between alleles of hsl7 and kel1, which arose together in a low-frequency lineage. [Emphasis added.]
Their prime example of “intracohort synergistic epistasis” (e.g., two mutations that interact somehow) as a case of adaptive evolution fails tests #1 and #2. All they notice is that the alleles localize to the poles of the yeast cell somehow, but they don’t know why. As expected, most of the mutations are neutral, or have effects that are so small as to get lost in the noise. Let’s cut to the chase and look for innovation or novelty:
Deletion of HSL7 is deleterious under a wide range of conditions, including the rich glucose media used here; thus our data suggest that the evolved hsl7 allele bestows a novel function or alters an existing function. Extensive characterization of such rare beneficial mutations requires long-term high-replicate evolution experiments followed by comprehensive analysis linking genotype to phenotype. Likely due to their large target size, loss-of-function mutations dominate adaptive evolution experiments, though rare beneficial mutations and epistatic interactions may provide the raw material for molecular innovation in natural populations.
Do they identify a new function? No; they might have just found a mutation that “alters an existing function.” All they know is without it, the effects are “deleterious” somehow, but they don’t know what the allele is doing. They tell us that beneficial mutations are rare, and that adaptive evolution experiments are dominated by loss-of-function mutations. Don’t look for a new wing or eye emerging in this paper. Instead: rare beneficial mutations and epistatic interactions “may” provide the “raw material” for innovations in natural populations. Their lab culture, we notice too, is not a natural population.
So that was the only use of the word “innovation” in the paper: a lone suggestion that some beneficial mutation or interacting set of mutations “may provide the raw material” for innovation someday over the rainbow. And how did they measure the adaptive fitness of all those alleged “beneficial mutations” they talk about? Look in the Materials & Methods section: they measured it by survival. Tautological evolution rears its lovely head again.
We should briefly consider the possibility that survival might reduce fitness. Imagine a population of yeast cells that divides recklessly, like cancer. Say there’s an organism in the natural environment that likes the taste of those mutated, rapidly dividing yeast cells and snacks on them. You’re not going to know that in the lab. Lenski and this team will just measure them out-competing other strains, and assume they are adaptive. What we are looking for is proof of a chance mutation that produces a new, useful, novel, innovative function. That is not in evidence here.
Resurrecting Lost Innovations
Let’s try another paper. Phys.org tells about a research team that tried to re-create the Precambrian version of beta-lactamase. If that enzyme sounds familiar, it’s because Biologic Institute scientist Douglas Axe did work on beta lactamase to measure the tolerance of protein folds to mutation. These researchers approach the enzyme from an evolutionary angle, seeing if the supposed primitive form of beta-lactamase might have been capable of finding a new active site.
The first question should be, how can they “resurrect an ancient protein”? This is where the circular reasoning comes in. “By comparing today’s sequences to each other within an evolutionary framework, scientists can reasonably infer the sequence of an ancestral protein from which the modern versions descended using models of sequence evolution.” So they will try to infer evolution within an evolutionary framework. Guess what they will find! Obviously, with different assumptions, one could come to completely different conclusions. If you compared the ignition from a Toyota, a Ford, a Cadillac, and a John Deere tractor “within an evolutionary framework,” how solid would your model of a “Precambrian” ignition be?
They announce that the Precambrian enzyme was more malleable (their word is “promiscuous”) than the modern beta lactamase enzymes, which they assume have become less tolerant to change as they became more specialized. So when they constructed the mythical Precambrian enzyme, lo and behold, it could find a new active site!
“We have found that a minimalist design to introduce a de novo activity (catalysis of the Kemp elimination, a common benchmark in de novo enzyme design) fails when performed on modern β-lactamases, but is highly successful when using the scaffolds of hyperstable/promiscuous Precambrian β-lactamases,” says Eric A. Gaucher from the Institute for Bioengineering and Biosciences, Georgia Institute of Technology.
Well, that’s great. We might expect our mythical Precambrian ignition could also tolerate more types of keys. Would that make it more innovative? Hardly; it would be less secure! The Kemp elimination reaction is only a test of whether the engineered enzyme can extract a proton from a carbon atom; it is “a non-natural reaction that is unknown to biological organisms.” Engineers use the test for “rational enzyme design.” Apparently, “lack of a selective pressure to generate Kemp elimination activity during evolution” indicates it is a useless activity for real living organisms. Notice that the paper in Nature Communications doesn’t even mention innovation or novelty, but begins with a statement of Darwinian faith:
Protein engineering studies often suggest the emergence of completely new enzyme functionalities to be highly improbable. However, enzymes likely catalysed many different reactions already in the last universal common ancestor. Mechanisms for the emergence of completely new active sites must therefore either plausibly exist or at least have existed at the primordial protein stage.
The best part may be the opening two paragraphs. Notice that after all these years, nobody has a good case of an enzyme evolving a new active site. Watch them also call it a huge unsolved problem in molecular evolution, and admit that everybody knows that finding a new functional active site is highly improbable. Note lastly how much intelligent design has factored into their efforts to solve the problem:
Enzyme activity is determined by the structure of a particular region of a protein called the active site. The generation of completely new active sites capable of enzyme catalysis is, arguably, one of the most fundamental unsolved problems in molecular biology.
Rational and modern design approaches to this problem have been developed using complex computational methods, but without conclusive results. Indeed, protein engineering studies often suggest that the emergence of completely new enzyme active sites is highly improbable.
But in the actual paper, they do not demonstrate any new active site with a clear functional advantage — certainly not by chance, since they inserted their engineering hands into the work:
Here, we use resurrected Precambrian proteins as scaffolds for protein engineering and demonstrate that a new active site can be generated through a single hydrophobic-to-ionizable amino acid replacement that generates a partially buried group with perturbed physico-chemical properties. We provide experimental and computational evidence that conformational flexibility can assist the emergence and subsequent evolution of new active sites by improving substrate and transition-state binding, through the sampling of many potentially productive conformations.
In essence, they engineered a mythical Precambrian enzyme by intelligent design, and found a way to make it promiscuous. That dog won’t hunt. Instead, we find that Doug Axe is vindicated again; the team admits that finding a new active site is highly improbable. The only reason they believe they “emerged” by chance is because they exist. (See faulty answer #3 again.)
One more angle: the hunt for clear evidence of an innovation arising in the fossil record. David Klinghoffer just wrote about the “Rangeomorph bang” in the Ediacaran fossil record, the sudden appearance of large frond-like extinct organisms before the Cambrian explosion. Here’s another Ediacaran critter called Cloudina (see our discussion in March of this simple creature). A paper in Nature Scientific Reports looks into “Ecological interactions in Cloudina from the Ediacaran of Brazil: implications for the rise of animal biomineralization.” The word “innovation” appears three times here, so let’s look for a true chance innovation.
- At the Ediacaran/Cambrian boundary, ecosystems witnessed an unparalleled biological innovation: the appearance of shelled animals.
- The Ediacaran Period (635–541 Ma) was marked by the record of enigmatic macroscopic organisms. This time interval embraces the first record of fossilized animals, including biomineralizers (e.g., Namacalathus, Cloudina), and vagile bilateria (e.g., Kimberella), as well as their innovative ecological interactions, such as macrophagous predation and competition.
- Biomineralization among animals was one of the most impactful innovations in the history of life, and it affected sedimentological regimes and biogeochemical cycles and led to the complexification of benthic ecosystems and ecological interactions.
Unfortunately, all the talk of innovation here falls under the third fallacy we discussed in the opening: ideological assumptions. Their evidence boils down to, “It’s there, design is verboten, therefore it evolved.”
These evolutionary novelties led to the escalation and systematic organization of food webs, guilds and niches during the Cambrian radiation. It was the dawn of animal life.
The Rhapsody in Blue performance was nice, but we came for the magic act. We were looking for a rabbit to emerge out of a hat without a magician. We found a pre-existing rabbit and a hat, but no connection between the two.
In summary, we went looking for evidence of true innovation by chance. Evolutionists desperately tried to provide examples, but each time vanished in a cloud of suggestions. All prospective examples fell into the three faulty answers that disqualify them as scientific.
What really impressed us were the frequent admissions that the emergence of novel function is highly improbable, and “one of the most fundamental unsolved problems in molecular biology” — evolutionary molecular biology, that is.
Image credit: Courtesy of Illustra Media, from Origin: Design, Chance and the First Life on Earth.