Search for: All records

ABSTRACT Organisms can react to environmental variation by altering their phenotype, and such phenotypic plasticity is often adaptive. This plasticity contributes to the diversity of phenotypes across the tree of life. Generally, the production of these phenotypes must be preceded by assessment, where the individual acquires information about its environment and phenotype relative to that environment, and then determines if and how to respond with an alternative phenotype. The role of assessment in adaptive plasticity is, therefore, crucial. In this Review, we (1) highlight the need for explicitly considering the role of assessment in plasticity; (2) present two different models for how assessment and the facultative production of phenotypes are related; and (3) describe an overarching framework for how assessment evolves. In doing so, we articulate avenues of future work and suggest that explicitly considering the role of assessment in the evolution of plasticity is key to explaining how and when plasticity occurs. Moreover, we emphasize the need to understand the role of assessment in adaptive versus maladaptive plasticity, which is an issue that will become increasingly important in a rapidly changing world. 

Agrowing number of studies have applied evolutionary and ecological principles to understanding cancer.However, few such studies have examined whether phenotypic plasticity––the ability of a single individual or genome to respond differently to different environmental circumstances––can impact the origin and spread of cancer. Here, we propose the adaptive horizontal transmission hypothesis to explain how flexible decision-making by selfish genetic elements can cause them to spread from the genome of their original host into the genomes of other hosts through the evolution of transmissible cancers. Specifically, we hypothesize that such cancers appear when the likelihood of successful vertical transmission is sufficiently low relative to the likelihood of successful horizontal transmission. We develop an evolutionary optimization model of this hypothesis, highlight empirical findings that support it, and offer suggestions for future research. Generally, phenotypically plastic selfish genetic elements might play an important role in the evolution of transmissible cancers. 

Many organisms facultatively produce different phenotypes depending on their environment, yet relatively little is known about the genetic bases of such plasticity in natural populations. In this study, we describe the genetic variation underlying an extreme form of plasticity––resource polyphenism––in Mexican spadefoot toad tadpoles, Spea multiplicata. Depending on their environment, these tadpoles develop into one of two drastically different forms: a carnivore morph or an omnivore morph. We collected both morphs from two ponds that differed in which morph had an adaptive advantage and performed genome-wide association studies of phenotype (carnivore vs. omnivore) and adaptive plasticity (adaptive vs. maladaptive environmental assessment). We identified four quantitative trait loci associated with phenotype and nine with adaptive plasticity, two of which exhibited signatures of minor allele dominance and two of which (one phenotype locus and one adaptive plasticity locus) did not occur as minor allele homozygotes. Investigations into the genetics of plastic traits in natural populations promise to provide novel insights into how such complex, adaptive traits arise and evolve.