Genetic Regulation of Phenotypic Plasticity and Canalisation in Yeast Growth

Abstract

The ability of a genotype to show diverse phenotypes in different environments is called phenotypic plasticity. Phenotypic plasticity helps populations to evade extinctions in novel environments, facilitates adaptation and fuels evolution. However, most studies focus on understanding the genetic basis of phenotypic regulation in specific environments. As a result, while it’s evolutionary relevance is well established, genetic mechanisms regulating phenotypic plasticity and their overlap with the environment specific regulators is not well understood. Saccharomyces cerevisiae is highly sensitive to the environment, which acts as not just external stimulus but also as signalling cue for this unicellular, sessile organism. We used a previously published dataset of a biparental yeast population grown in 34 diverse environments and mapped genetic loci regulating variation in phenotypic plasticity, plasticity QTL, and compared them with environment-specific QTL. Plasticity QTL is one whose one allele exhibits high plasticity whereas the other shows a relatively canalised behaviour. We mapped phenotypic plasticity using two parameters–environmental variance, an environmental order-independent parameter and reaction norm (slope), an environmental order-dependent parameter. Our results show a partial overlap between pleiotropic QTL and plasticity QTL such that while some plasticity QTL are also pleiotropic, others have a significant effect on phenotypic plasticity without being significant in any environment independently. Furthermore, while some plasticity QTL are revealed only in specific environmental orders, we identify large effect plasticity QTL, which are order-independent such that whatever the order of the environments, one allele is always plastic and the other is canalised. Finally, we show that the environments can be divided into two categories based on the phenotypic diversity of the population within them and the two categories have differential regulators of phenotypic plasticity. Our results highlight the importance of identifying genetic regulators of phenotypic plasticity to comprehensively understand the genotype-phenotype map.

The Genomic Architecture of Interactions Between Natural Genetic Polymorphisms and Environments in Yeast Growth

“…We analyzed the later data (Bloom et al 2015), only to verify the key findings from the earlier data. Note that several yeast studies mapped growth rate QTLs in each of an array of environments (Cubillos et al 2011;Ehrenreich et al 2012;Bloom et al 2013;Wilkening et al 2014), or mapped plasticity QTLs across environments (Yadav et al 2016), but these studies either treated growth rates in different environments as different traits, or treated growth rate variance among environments as a phenotypic trait. Hence, yeast G3E in growth rate has not been studied.…”

Quantified ensemble 3D surface features modeled as a window on centric diatom valve morphogenesis

“…Phenotype during development may be studied in unicellular organisms with regard to epistasis (e.g., Sanjuán and Elena 2006) and canalization (e.g., Yadav et al 2016). The processes of epistasis and canalization concerning the genotype may be extended to understand interactions among quantified characters of the phenotype in models of development (Rice 1998).…”

Epithelial-mesenchymal plasticity: How have quantitative mathematical models helped improve our understanding?

“…However, during tumor progression, many of the molecular brakes against phenotypic plasticity are deregulated, enabling cancer cells to behave as 'moving targets' that can play 'hide-and-seek' with multiple therapeutic regimes (Roesch, 2015;Varga et al, 2014). In addition, these phenotypic conversions can facilitate adaptation by enabling geneticallyidentical cells to exhibit a diverse set of phenotypes and may also help fuel genetic evolution of cancer cells (Brooks et al, 2015;Mooney et al, 2016;Yadav et al, 2016).…”