PMID: 17720926;PMCID: PMC2034656;Abstract:
Phenotypic loss is an important evolutionary force in nature but the mechanism(s) responsible for loss remains unclear. We used both simulation and multiple-regression approaches to analyze data on the loss of sporulation, a complex bacterial developmental process, during experimental evolution of Bacillus subtilis. Neutral processes of mutational degradation alone were sufficient to explain loss-of-sporulation ability in four of five populations, while evidence that selection facilitated mutational loss was found for only one population. These results are discussed in the context of the evolution of sporulation in particular and phenotypic loss in general. Copyright © 2007 by the Genetics Society of America.
Evolutionary biology has a complex relationship with ideas of chance, purpose, and progress. Probability plays a subtle role; strikingly, founding figures in statistics were motivated by evolutionary questions. The findings of evolutionary biology have been used both in support of narratives of progress, and in their deconstruction. Likewise, professional biologists bring to their scientific work a set of preconceptions about chance and progress, grounded in their philosophical, religious, and/or political views. From the religious side, questions of purpose are ever-present. We explore this interplay in five broad categories: chance, progress, intelligence, eugenics, and the evolution of religious practices, each the subject of a semester long symposium. The intellectual influence of evolutionary biology has had a broad societal impact in these areas. Based on our experience, we draw attention to a number of relevant facts that, while accepted by experts in their respective fields, may be unfamiliar outside them. We list common areas of miscommunication, including specific examples and discussing causes: sometimes semantics and sometimes more substantive knowledge barriers. We also make recommendations for those attempting similar dialogue.
PMID: 19917766;PMCID: PMC2828720;Abstract:
Epigenetically inherited aggregates of the yeast prion [PSI+] cause genomewide readthrough translation that sometimes increases evolvability in certain harsh environments. The effects of natural selection on modifiers of [PSI+] appearance have been the subject of much debate. It seems likely that [PSI+] would be at least mildly deleterious in most environments, but this may be counteracted by its evolvability properties on rare occasions. Indirect selection on modifiers of [PSI+] is predicted to depend primarily on the spontaneous [PSI+] appearance rate, but this critical parameter has not previously been adequately measured. Here we measure this epimutation rate accurately and precisely as 5.8 × 10-7 per generation, using a fluctuation test. We also determine that genetic "mimics" of [PSI1] account for up to 80% of all phenotypes involving general nonsense suppression. Using previously developed mathematical models, we can now infer that even in the absence of opportunities for adaptation, modifiers of [PSI+] are only weakly deleterious relative to genetic drift. If we assume that the spontaneous [PSI+] appearance rate is at its evolutionary optimum, then opportunities for adaptation are inferred to be rare, such that the [PSI+] system is favored only very weakly overall. But when we account for the observed increase in the [PSI+] appearance rate in response to stress, we infer much higher overall selection in favor of [PSI+] modifiers, suggesting that [PSI+]-forming ability may be a consequence of selection for evolvability. Copyright © 2010 by the Genetics Society of America.
PMID: 10866229;Abstract:
Viral load fluctuates during the natural course of asymptomatic HIV-1 infection. It is often assumed that these fluctuations are random around a set point or underlying growth trend. Using longitudinal data, we tested whether fluctuations in viral load can be better explained by changes in CD4+ T-cell count than by a set point or trend of exponential growth. The correspondence between viral load and CD4+ T-cell count could be described by a simple mathematical relation. Using a bootstrapping approach, the hypothesis that viral load fluctuations are random around a set point was rejected with p .00005. The hypothesis that viral load fluctuations are random around a trend of exponential growth was rejected with p .005. Viral load data was explained better by changes in CD4+ T-cell counts than by a set point or by a trend of exponential growth. The implications of this finding for improved prognostication discussed.
PMID: 17099057;PMCID: PMC1808353;Abstract:
A possible origin of novel coding sequences is the removal of stop codons, leading to the inclusion of 3′ untranslated regions (3′ UTRs) within genes. We classified changes in the position of stop codons in closely related Saccharomyces species and in a mouse/rat comparison as either additions to or subtractions from coding regions. In both cases, the position of stop codons is highly labile, with more subtractions than additions found. The subtraction bias may be balanced by the input of new coding regions through gene duplication. Saccharomyces shows less stop codon lability than rodents, probably due to greater selective constraint. A higher proportion of 3′ UTR incorporation events preserve frame in Saccharomyces. This higher proportion is consistent with the action of the [PSI+] prion as an evolutionary capacitor to facilitate 3′ UTR incorporation in yeast. © 2006 The Authors.
