Statistical Inference on the Mechanisms of Genome Evolution
Michael Lynch*
Department of Biology, Indiana University, Bloomington, Indiana, United States of America
Citation: Lynch M (2011) Statistical Inference on the Mechanisms of Genome Evolution.
PLoS Genet 7(6): e1001389. doi:10.1371/journal.pgen.1001389
Editor: Nancy A. Moran, Yale University, United States of AmericaPublished: June 9, 2011Copyright: © 2011 Michael Lynch.
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: The author acknowledges the National Science Foundation, National Institutes of Health, and the Department of Defense for financial support.
The funders had no role in the preparation of the article.
Competing interests: The author has declared that no competing interests exist.*
E-mail: milynch@indiana.edu
Introduction
In a series of publications, I and my colleagues have developed hypotheses for how the evolution of various aspects of genome architecture is expected to proceed under conditions in which the forces of random genetic drift and mutation predominate (e.g., [1]–[15]). These models, collectively referred to below as the mutational-hazard (hereafter, MH) hypothesis, are sometimes represented as neutral models [16], [17], but this is not correct, as the key component of each model is the deleterious mutational consequence of excess DNA. The MH hypothesis is, however, a nonadaptational model, in that it yields expectations on the structure of genomes without invoking external selective forces. It is likely that some aspects of these models will need to be changed as more is learned about the molecular consequences of various aspects of gene structure and the nature of mutation. Such modifications will not alter the need for baseline null hypotheses in attempts to defend adaptive explanations for variation in genomic architecture [9]. Nevertheless, any theory that strives to provide a unifying explanation for diverse sets of genomic observations must be scrutinized extensively from a variety of angles and interpreted in the context of well-established molecular and population-genetic processes. Although I will argue that a recent challenge to the MH hypothesis by Whitney and Garland ([18]; hereafter, WG) contains numerous problems, this exchange may help clarify more broadly misunderstood issues.
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