If I asked you what drives evolution, what are the first things that come to mind? If you are like me, it is mutation and natural selection. That is what we are taught in school and that is what we read about on the popular level and hear in most popular-level discussions. Now, what if I told you that prominent evolutionary biologists dissent from this view, or at least significantly modify it. We will explore a case of this dissent in this blog post.
A while back I was interested to revisit the arguments for Intelligent Design (ID) and was led down an alternate path. Out of all the ID arguments out there, one that strikes me as particularly difficult and nagging is the problem of generating new biological information. This can be stated as: natural selection tells us how genes survive, but not how they arrive. How do genes and phenotypes arrive on the scene? Again, if you are anything like me, you’ve heard it so many times that it is the mantra we all adhere to: microevolution working on an epochal timescale equals macroevolution. That’s it. But, this time I began wondering if this assertion is really plausible. We now have tools to examine the plausibility thanks to the molecular revolution.
From my own searches I could find virtually nothing that directly addresses this question, so I decided to seek out the most qualified scientists and read their material on the subject. That is when I learned about Michael Lynch, an emeritus professor, member of the Academy, and author of a textbook on population genetics. We will be examining select arguments from Lynch’s paper, “The Frailty of Adaptive Hypotheses for the Origins of Organismal Complexity”. (1) From the outset Lynch sets up the problem that at its core is ID’s nagging question, where does new genetic information come from? This is considered in terms of genomic complexity and finally organismal complexity as the title states. Early on in a moment of polemical gold he states:
It has long been known that natural selection is just one of several mechanisms of evolutionary change, but the myth that all of evolution can be explained by adaptation continues to be perpetuated by our continued homage to [Charles] Darwin’s treatise in the popular literature. For example, [Richard] Dawkin’s agenda to spread the word on the awesome power of natural selection has been quite successful, but it has come at the expense of reference to any other mechanisms. . .
He goes on to explain that there are four primary forces of evolution: natural selection, mutation, genetic drift, and recombination. Only the first is adaptive, therefore the remaining forces are nonadaptive.
Lynch frequently utilizes differences between prokaryotes and eukaryotes to understand the origin of complexity, so we will review these briefly. Let’s start with morphologic differences. Prokaryotes are unicellular organisms that are relatively small, lack a nuclear membrane, have a capsule, and flagellum for motility. Think bacteria. Next, eukaryotes can be unicellular (yeast) or multicellular (animals) and have relatively larger cells, nuclear membrane present, usually no capsule, and no flagellum. In multicellular organisms, cells differentiate to take on specific functions such as nervous tissue, muscle, connective tissue, absorptive epithelium in the gut, endocrine cells, and so on. Notice that morphologically eukaryotes can be vastly more complex. Prokaryotes represent an earlier phase in evolutionary history compared to eukaryotes, thus complexity developed over evolutionary history leading to our modern biosphere. This complexity is mirrored on the genomic level. Eukaryotic genomes contain an abundance of mobile elements, genes with multiple introns, multiple transcription-factor binding sites, preservation of gene duplications, and genes which are transcribed into units with untranslated flank sequences (i.e., poly A tail). Prokaryotic genomes do not contain any of these thus are streamlined by comparison, and this is main point you should get from this.
Recall the Central Dogma of Biology: biological information flows from gene to phenotype and the starting point is the gene. This means that if we understand the origins of genomic complexity (i.e. from prokaryotes to eukaryotes), we understand the origins of complexity on other levels of biological organization such as morphology, multicellularity, size, function, and so on. This is what the molecular revolution affords us. So, the central question is, what evolutionary forces are primarily responsible for producing complexity?
Lynch argues for the “passive emergence of genome complexity by nonadaptive processes”. That is a mouthful, so take a minute to digest each term. Passive meaning no one is tampering with it (i.e., no intelligent agent). Nonadaptive processes meaning mutation, genetic drift, and recombination as opposed to the adaptive process of natural selection. Alright folks, here is the bad news. The bad news is Lynch’s argument hinges on population genetic theory which is a bit technical. I am not going to derive population genetic theory here, however suffice it to say that nonadaptive processes predominate (over natural selection) when 2Ngs << 1 where Ng is the effective population size and s is the fractional selection advantage. This is also called the “criterion for effective neutrality” with neutrality referring to nonadaptive and non-deleterious. Further substituting in the equation, s = nu where n is number of nucleotides to be conserved for proper gene function and u is the mutation rate per nucleotide site. Notice that as s increases so does n (they are directly proportional), which means that each adaptive embellishment comes with the cost of maintaining the fidelity of more nucleotides. This is called mutation hazard. Using population genetic data to calculate real numbers for the criterion for effective neutrality, we find that:
. . . an embellishment that increases the mutational target size of a vertebrate by n<250 will be largely immune from selection, and hence free to drift to fixation, whereas the critical value of n for a prokaryote is << 10.
In simplified terms, vertebrates have a markedly easier time increasing the complexity of their genome without mutational hazard whereas prokaryotes have a difficult time. Recall the differences in complexity between prokaryote and eukaryote genomes. The criterion of neutrality provides a powerful explanation for the observed differences. The differences are explained by neutral or nonadaptive increases in complexity. This, in a nutshell, is Lynch’s argument for the passive emergence of genome complexity by nonadaptive processes.
Lynch points out that even if one was not convinced that complexity primarily emerges from nonadaptive processes, these provide the null hypothesis. I find this interesting, and wonder how to go about establishing this from a philosophy of science point of view. Should the null hypothesis be totally random nonadaptive evolution and the adaptationists shoulder the burden of proof, or something else? (If anyone has an insight or has studied the philosophy of science, please indulge us). Lynch also points out frequently that there is no direct evidence for adaptive hypotheses. This makes his case stronger.
Lynch’s paper has a frustrated tone that suggests a broad failure of engagement with data and arguments for nonadaptive evolution. For example:
Most biologists are so convinced that all aspects of biodiversity arise from adaptive processes that virtually no attention is given to. . . neutral evolution, despite the availability of methods to do so. Such religious adherence to the adaptationist paradigm has been criticized as being devoid of intellectual merit [citing a paper by Stephen Jay Gould and Richard Lewontin].
The hypothesis that expansions in the complexity of the genomic architecture are largely driven by nonadaptive evolutionary forces is capable of explaining a wide range of previously disconnected observations. . . This theory may be viewed as overly simplistic. However, simply making the counterclaim that natural selection is all-powerful (without any direct evidence) is not much different from invoking an intelligent designer (without any direct evidence).
There are likely to be scientists who understand these arguments and know the data yet disagree. However, there are also probably scientists who simply avoid mathematical theories, as biologists are infamous for. And, there are also scientists whose careers or reputations hang on the power of natural selection, so they have motivations to dismiss or sidestep engagement. What Lynch seems to press in this paper is more serious and objective engagement.
Let us revisit ID’s nagging question: how is new biological information introduced? Is this plausible? It seems the answer is, complexity accrues primarily through nonadaptive forces which is also called neutral evolution. When neutral evolution was first worked out in the 80’s Kimura coined the term “survival of the luckiest” to counter adaptationist’s term “survival of the fittest”. (2) And, this is where I ask my dear readers:
How lucky are we?
1) Lynch M. “The frailty of adaptive hypotheses for the origins of organismal complexity.” Proc Natl Acad Sci USA. 2007 May 17;104 Suppl 1:8597-604. Free full text.
2) Kimura M. “The neutral theory of molecular evolution and the world view of the neutralists.” Genome. 1989;31(1):24-31. PMID: 2687096.