Compounding Complexity Passively

May 18th, 2007 Placozoan Posted in News |

I THOROUGHLY AGREE with the statement “it is well known that most biologists abhor all things mathematical” given in the article that I will cover today. The author deals with population genetics, and speeds through some basic equations in a page and a half. I will certainly not be talking about any equations today, but will attempt to restate the concepts in this fascinating paper.

The author, Michael Lynch, rejects the idea that organismal complexity arose through an adaptive mechanism (I previously discussed another paper suggesting a nonadaptive mechanism here). Key in his paper is an analysis of the differences between prokaryote and eukaryote evolution.

Compared to prokaryotic genomes, eukaryotic genomes are complicated and contain a lot of genetic detritus. Genes are divided into introns and have large 5′ untranslated regions and many transcription factor binding sites. The genome contains multiple parasitic mobile elements. Prokaryotes are comparatively neat and organized. Their genes are almost always intron-less, and they don’t have the number of parasitic mobile elements that eukaryotes do. Previously it has been thought that metabolic requirements or body plan limitations kept prokaryotes from compounding the amount of genetic material that eukaryotes have, but Lynch suggests a different reason.

Lynch points out that each addition of DNA to a gene increases the odds that a harmful mutation will inactivate the gene. Any addition to a gene is unlikely to be immediately beneficial, so either the mutated allele will be removed shortly by natural selection if harmful, or if it is neutral it may proceed to fixation or elimination by genetic drift.

Next, Lynch discusses the process of genetic drift and population size. While there are about 6.5 billion humans on the planet, there are more than 6.5 billion bacteria in only 50 mL of a log phase culture. The difference in effective population size causes genetic drift to be much less tolerant in bacterial populations, so fixation of a neutral allele can take impractically long time periods and usually elimination results. However, in the small populations of eukaryotes, genetic drift is more prone to fix neutral alleles, and larger additions to the genome are acceptable. Lynch calculates that in most prokaryote populations a mutation adding fewer than 10 bp can escape elimination by selection and possibly be fixed by genetic drift, but in vertebrates that number is closer to 250 bp. Thus it appears that the reason that prokaryotic genomes are so comparatively simple is intolerance for genetic additions and slow fixation by genetic drift due to large population size, while eukaryotic genomes are more complex because they are more free to add genetic material and fix the changes rapidly because of their comparatively small population sizes.

So how do we integrate the passive addition of genetic material with the undoubted positive selection we see for some phenotypes? Lynch says,

. . . to the extent that an increase in gene-architectural complexity is a precondition for the emergence of greater complexity at the organismal level (including the hallmarks of multicellularity: multiple cell types, complex patterns of gene expression, and mechanisms of cell signaling), a long-term synergism may exist between nonadaptive evolution at the DNA level and adaptive evolution at the phenotypic level. There is no need to abandon the idea that many of the external morphological and/or behavioral manifestations of multicellularity in today’s organisms are adaptive.

To clarify this, Lynch gives three examples of how specialized gene function can emerge. First, a gene initially under a single transcription factor controlling expression in all tissues may compile additional transcription factors that are tissue-dependent. Degradation of the now redundant initial transcription factor leaves the gene with a more complex regulatory system. Secondly, the regulatory region of this gene may duplicate, then the duplicates undergo changes to control transcription in different tissues. Finally, when an entire gene duplicates the duplicates are then free to evolve to suit different roles, as is the case with the human hemoglobin genes.

The final example is that of a gene product cascade, in which an upstream gene activates a downstream one, which then may either activate another or terminate the chain by producing the final phenotypic result (similar to the clotting cascade). In this case, an initially self-regulating gene may develop redundant regulation by an upstream gene, and can then either lose this redundant regulation or lose self-regulation without harm. If it loses self-regulation it has become the final gene in a cascade, and additional genes may be added upstream by the same mechanism.

These mechanism provide a way in which underlying genetic mechanisms may reorganize, yet the fitness of the organism is unchanged while the new systems evolve.

Thus, the new regulatory architecture emerges beneath a constant phenotype, without any bottleneck in fitness during the transitional phase of mixed genotypes. Such neutral transitions may help explain apparent cases of ‘‘developmental system drift,’’ whereby closely related species achieved similar morphological structures by substantially different mechanisms (59, 63, 71–74).

It cannot escape my notice that this elegant mechanism once again refutes two of the most common creationist and Intelligent Design claims, that any additions to the genome must be immediately beneficial and that such complex systems are irreducibly complex.

Lynch, M. “The failty of adaptive hypotheses for the origins of organismal complexity.” Proceedings of the National Academy of Sciences, USA 2007, 104, Suppl. 1, 8597.