Looking back at the evolution of cells prior to the expansion of multi-cellularity, there was the advent of the eukaryotic cell. How did it arise? The concept of endosymbiosis is of course a well-known theory on the origins of the eukaryotic cell, but what about the genetic structure itself? One of the leading thinkers in this area appears to be Michael Lynch, who recently penned a review in Molecular Biology and Evolution on The Origins of Eukaryotic Gene Structure. In this review Lynch addresses the correlation between genomic complexity and organismal complexity, proposing that the early developments of complexity are driven primarily by non-adaptive stochastic forces, rather than by Natural Selection alone. He draws support from observations of a general negative relationship between selection efficiency and genome complexity, and while this concept is rather speculative, it shows great appeal as a plausible alternative – afterall, how can we explain how “intron splicing, untranslated regions, modular regulatory elements, and expansive intergenic regions that harbor diffuse control mechanisms” might have been selected for?
As his alternative, Lynch proposes that random genetic drift and mutational pressures account for the acquired robustness and diversity of storage of genetic information – something very much echoed by observations on gene duplication in divergence of protein-DNA interactions, and evolution of digital organisms and computer viruses.
Of course Lynch doesn’t completely dismiss Natural Selection, but adaptive mechanisms along the strict Darwinian or Modern Synthesis modes are insufficient to explain the genome-wide changes. Put more succinctly:
… it is worth emphasizing that the goal here is not to explain the expression of a gene in a new temporal or spatial context, but to understand how a gene that is initially under control of a ubiquitously expressed transcription factor comes to be regulated by spatially and/or temporally restricted transcription factors while initially retaining the same overall expression pattern. The process envisioned, subfunction fission, invokes gradual structural modifications of preexisting enhancers within a gene (descent with modification) rather than the saltatory appearance of entirely new regulatory modules (Force et al., 2005). Subfunction fission involves consecutive phases of regulatory-region expansion and contraction.
Here, Lynch’s “gradual structural modifications of preexisting enhancers” clearly has appeal in justifying a stochastic or drift-driven acquisition of complexity, but what does he mean by mutational pressure as the other driver of complexification? He explains this with his findings on the genomic perils of increased organism size, which cause substantial reductions in the efficiency of natural selection. This makes sense for a couple reasons that can be reduced to a discussion on how easily it is for mutations to generate variation in eukaryotes versus prokaryotes – it’s easy to see that prokaryotes have an enormous potential for generating diversity in a population, the reverse of which is the benefit eukaryotes gain when they acquire new mechanisms of converting mutations (be they base-subsituted or transposed mutations) to the phenotypic level for adaptive selection to act upon. This is an intuitive (if complex) concept, suggesting an origin for what is now popularly referred to as epigenetics, or multiple levels of regulation for gene expression.
This may be tough for some to wrap their head around, but the over-riding theme in the Natural Selection v. Neutral Theory debate is that life works on a mixture of stochastic (genetic drift) and deterministic (adaptive selection) forces to generate phenotypic diversity at a rate fast enough to survive in a world of limited resources and harsh conditions.
As I mentioned towards the top, related principles of self-managing complexity in reproducing populations has been demonstrated by work in genetic algorithms and digital organisms. It’s interesting, I think, that some individuals seize upon related concepts to promote a “Front-loading” explanation for Intelligent Design, but this is an illogical argument — it rests upon the presupposition that both the mathematical rules of complex systems and the origin of life have as their causation a higher power: a wildly speculative view that sees what it wants to see.
- The origins of eukaryotic gene structure. Lynch M. Mol Biol Evol. 2006 Feb; 23(2):450-68.
- The origin of subfunctions and modular gene regulation. Force A, Cresko WA, Pickett FB, Proulx SR, Amemiya C, Lynch M. Genetics. 2005 May; 170(1):433-46.
For more reading, I recommend looking up Motoo Kimura’s 1983 book “The Neutral Theory of Molecular Evolution,” Susumu Ohno’s 1970 book “Evolution by Gene Duplication,” and topics on “Digital Organisms.”