Project description:Analysis of evolved changes in transcriptional plasticity and parental effects on plasticity induced by mild heat stress in the nematode Caenorhabditis remanei. Results of this study highlight the importance of the broad environmental context of an organism and its influence on phenotypic plasticity, parental effects, and evolutionary responses.
Project description:Analysis of evolved changes in transcriptional plasticity and parental effects on plasticity induced by mild heat stress in the nematode Caenorhabditis remanei. Results of this study highlight the importance of the broad environmental context of an organism and its influence on phenotypic plasticity, parental effects, and evolutionary responses. mRNA profiles of ancestral and two experimentally evolved populations of C. remanei. Parents of the sampled worms were raised at either 20°C or 30°C, then the resulting embryos were divided and reared at either 20°C or 30°C prior to collection (as L1 larvae). 6 replicates/larval temperature for each population if the parents were raised at 20°C, and 2 replicates/larval temperature for each population if the parents were raised at 30°C.
Project description:Analysis of constitutive changes in gene expression patterns in populations of the nematode Caenorhabditis remanei experimentally evolved to either acute heat stress, acute oxidative stress or the lab environment. Results of this study demonstrate that acute heat stress and acute oxidative stress are complex traits with a unique genetic basis. Overall design: Pooled population RNA sequencing libraries were obtained from the ancestor population and three evolved populations: one biological replicate of the control selected population, one heat stress selected population and one oxidative stress selected population per replicate. Tissue was collected from populations of L1 larval worms.
Project description:Many organisms can acclimate to new environments through phenotypic plasticity, a complex trait that can be heritable, subject to selection, and evolve. However, the rate and genetic basis of plasticity evolution remain largely unknown. We experimentally evolved outbred populations of the nematode Caenorhabditis remanei under an acute heat shock during early larval development. When raised in a non-stressful environment, ancestral populations were highly sensitive to a 36.8°C heat shock and exhibited high mortality. However, initial exposure to a non-lethal high temperature environment resulted in significantly reduced mortality during heat shock (hormesis). Lines selected for heat shock resistance rapidly evolved the capacity to withstand heat shock in the native environment without any initial exposure to high temperatures, and early exposure to high temperatures did not lead to further increases in heat resistance. This loss of plasticity would appear to have resulted from the genetic assimilation of the heat induction response in the non-inducing environment. However, analyses of transcriptional variation via RNA-sequencing from the selected populations revealed no global changes in gene regulation correlated with the observed changes in heat stress resistance. Instead, assays of the phenotypic response across a broader range of temperatures revealed that the induced plasticity was not fixed across environments, but rather the threshold for the response was shifted to higher temperatures over evolutionary time. These results demonstrate that apparent genetic assimilation can result from shifting thresholds of induction across environments and that analysis of the broader environmental context is critically important for understanding the evolution of phenotypic plasticity. mRNA profiles of ancestral and two experimentally evolved populations of C. remanei at 20°C or 30°C, 6 replicates/temperature for each population
