![]() ![]() ![]() Beach mouse subspecies on Florida’s Gulf and Atlantic coasts have independently evolved light coloration from a dark-colored mainland ancestor ( 21). One classic example of repeated color evolution involves beach mice in the southeastern United States. ![]() At the phenotypic level, color can vary dramatically in the wild, be measured straightforwardly, and have clear links to fitness ( 20). At the molecular level, the genes and pathways involved in vertebrate pigmentation have been well characterized ( 19). Variation in pigmentation has long served as a model for the study of adaptation. Thus, it remains difficult to determine the extent to which similar or different mutations contribute to repeated phenotypic evolution and where in the genome they occur. By contrast, coding mutations are generally more amenable to identification and functional validation therefore, when precise mutations have been shown to drive repeated evolution across species, they most commonly correspond to coding mutations ( 18). ![]() This is in part due to the complexity of gene regulatory landscapes and the relative difficulty in testing the effects of a noncoding allele ( 17). Nonetheless, when regulatory change has been implicated in repeated evolution, it is still rare that the causal regions, elements, or mutations have been identified ( 1, 16). 14) or combinations of both regulatory and coding changes ( 15) have been identified. Moreover, it has been argued that changes in cis-regulatory elements may be the primary substrate of adaptation ( 8– 10), although many examples of protein-coding changes (refs. Did similar phenotypes arise via the same or different molecular changes? While there are empirical examples of selection from new mutations ( 1– 3), it has been suggested that rapid adaptation, in particular within species, may be fueled by selection on the same alleles from preexisting genetic variation (refs. For example, one can ask the following question. Together, our results suggest that this identified Agouti enhancer allele has been maintained in mainland populations as standing genetic variation and from there, has spread to and been selected in two independent beach mouse lineages, thereby facilitating their rapid and parallel evolution.Ĭases of repeated evolution provide a particularly appealing context for understanding the drivers of adaptation. Notably, this same light allele appears fixed in both Gulf and Atlantic coast beach mice, despite these populations being separated by >1,000 km. Moreover, extended tracts of homozygosity in this Agouti region indicate that the light allele experienced recent and strong positive selection. Using a reporter-gene assay, we demonstrate that this regulatory region contains an enhancer that drives expression in the dermis of mouse embryos during the establishment of pigment prepatterns. We find that pigment variation is strongly associated with an ∼2-kb region ∼5 kb upstream of the Agouti signaling protein coding region. Next, in a uniquely variable mainland population ( Peromyscus polionotus albifrons), we scored 23 pigment traits and performed targeted resequencing in 168 mice. To facilitate genomic analyses, we first generated a chromosome-level genome assembly of Peromyscus polionotus subgriseus. Dorsal coats range from dark brown in mainland mice to near white in mice inhabiting sandy beaches this light pelage has evolved independently on Florida’s Gulf and Atlantic coasts as camouflage from predators. Here, we focus on the oldfield mouse ( Peromyscus polionotus), which occurs in the southeastern United States, where it exhibits considerable color variation. Identifying the genetic basis of repeatedly evolved traits provides a way to reconstruct their evolutionary history and ultimately investigate the predictability of evolution. ![]()
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