Academic journal article Genetics

Too Much of a Good Thing: The Unique and Repeated Paths toward Copper Adaptation

Academic journal article Genetics

Too Much of a Good Thing: The Unique and Repeated Paths toward Copper Adaptation

Article excerpt

IN his book, Wonderful Life (Gould 1989, p. 51), Stephen J. Gould famously opined that evolution is a historical and contingent process, so much so that "any replay of the tape would lead evolution down a pathway radically different from the road actually taken." While this is undoubtedly true when one considers the full complexity of an organism, refrains are often observed in evolution at the trait level. Repeated evolution, defined as "the independent appearance of similar phenotypic traits in distinct evolutionary lineages" (Gompel and Prud'homme 2009) has been documented in both ecological and clinical environments at all taxonomic levels, e.g., repeated loss of stickleback lateral plates in freshwater (Schluter et al. 2004), ecomorphs of Anolis lizards (Losos 1992), the acquisition of "cystic fibrosis lung" phenotypes in Pseudomonas aeruginosa in patients with cystic fibrosis (Huse et al. 2010), to name but a few. The development of sequencing technologies has recently allowed biologists to ask whether parallel genetic changes underlie observations of parallel phenotypic change. In some cases, parallel phenotypic evolution has been attributed to parallel genotypic evolution, for example, repeated changes to cis-regulatory regions of the same gene-the pigmentation gene yellow-underlie changes in wing pigmentation in male Drosophila (Prud'homme et al. 2006). At the other extreme are cases where different genetic targets underlie similar phenotypic shifts; for example, yeast adapting to rich media converged in fitness via a variety of genetic mechanisms (Kryazhimskiy et al. 2014), and beach mice adapting to sandy coastal dunes from the Gulf and Atlantic coasts of Florida converged in coat coloration via different mutations (Manceau et al. 2010). In such cases, unique evolutionary trajectories at the genetic level appear repeatable at the phenotypic level.

The degree of phenotypic repeatability is inherently linked with the genomic target size of appropriate mutations, with single-locus Mendelian traits with fewer target sites (and hence higher repeatability) at one extreme and quantitative traits at the other extreme. Even when multiple genes underlie a selected trait, however, there may be relatively few sites that, when mutated, have the magnitude of effect and sufficiently minor deleterious side effects to improve fitness overall (Stern 2013). Such pleiotropic constraints are thought to explain why cis-regulatory sites more often contribute to adaptation than trans-regulatory changes (Stern 2000; Gompel et al. 2005). The size of the population and the manner in which it reproduces are also critical. Large populations have access to rarer mutations, particularly those of large effect (Burch and Chao 1999), increasing the chance that the best of these mutations will fix in independent evolutionary trials (Bell and Collins 2008). Mutations with particularly high fitness are also more likely to fix in asexual populations, because clonal interference reduces the chance that minoreffect mutations establish (Rozen et al. 2002), unless adaptive mutations are so common that coalitions of mutations establish together (Fogle et al. 2008; Lang et al. 2013).

The nature and severity of environmental challenge will also affect the degree of repeatability at both the genotypic and phenotypic levels. If the environmental change is so severe that the population cannot replace itself and there are only a small fraction of mutations whose benefits are large enough to bring absolute fitness above one (Bell and Collins 2008), then adaptation would be more repeatable. On the other hand, if an organism is adapting via mutations whose effects are small relative to the distance to the fitness optimum, nearly half of mutations are predicted to be beneficial (Fisher 1930), and adaptation would be less repeatable. The genomic target size must also depend on the nature of mutations required: when adaptation can be accomplished by the loss of a function, adaptive mutations can potentially arise in any step along the pathway leading to that function via a variety of mechanisms [e. …

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