Genetic Regulation of Phenotypic Plasticity and Canalisation in Yeast Growth

  title={Genetic Regulation of Phenotypic Plasticity and Canalisation in Yeast Growth},
  author={Anupama Yadav and Kaustubh D. Dhole and Himanshu Sinha},
  journal={PLoS ONE},
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… 
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Phenotypic robustness determines genetic regulation of complex traits
This study demonstrates differential robustness as one of the central mechanisms regulating variation in populations and underlines its role in identifying missing heritability in complex phenotypes and diseases.
  • R. Wu
  • Biology, Environmental Science
    Evolution; international journal of organic evolution
  • 1998
The molecular genetic mechanisms for phenotypic plasticity across heterogeneous macro‐ and microenvironments were examined using the Populus genomic map constructed by DNA‐based markers and gene regulation was suggested to play a prevailing role in determining the norms of reaction to environments.
Yeast Growth Plasticity Is Regulated by Environment-Specific Multi-QTL Interactions
It is proposed that a targeted scan for epistatic interactions, such as the one described here, can help unravel mechanisms regulating phenotypic plasticity and contribute to the growth plasticity in yeast.
Genetics of phenotypic plasticity: QTL analysis in barley, Hordeum vulgare
Using both simulations and real data from barley, QTL mapping is used to obtain insights into the genetics of phenotypic plasticity, namely the phenotypesic variance across environments and the Finlay–Wilkinson's regression slope.
Adaptation to an extraordinary environment by evolution of phenotypic plasticity and genetic assimilation
  • R. Lande
  • Environmental Science
    Journal of evolutionary biology
  • 2009
Adaptation to a sudden extreme change in environment, beyond the usual range of background environmental fluctuations, is analysed using a quantitative genetic model of phenotypic plasticity, which indicates the optimal plasticity is proportional to the predictability of environmental fluctuations over time lag τ.
Rethinking phenotypic plasticity and its consequences for individuals, populations and species
It is claimed that rigorous testing of predictions requires methods that allow for quantifying and comparing whole organism plasticity, as well as the ability to experimentally manipulate the level of and capacity for developmental plasticity and phenotypic flexibility independent of genetic variation.
Mapping phenotypic plasticity and genotype–environment interactions affecting life-history traits in Caenorhabditis elegans
A genomewide single-nucleotide polymorphism map in a recombinant N2 × CB4856 inbred panel of the nematode Caenorhabditis elegans is used to study the genetic control of phenotypic plasticity to temperature in four fitness-related traits, that is, age at maturity, fertility, egg size and growth rate.
Differential Regulation of Antagonistic Pleiotropy in Synthetic and Natural Populations Suggests Its Role in Adaptation
It is proposed that during AP resolution, retaining the ability to vary signaling pathways such as Ras/PKA, may provide organisms with phenotypic flexibility, with increasing organismal complexity, because a partial resolution of AP could manifest as complex human diseases and the inability to resolve AP may play a role in speciation.
Assessing the complex architecture of polygenic traits in diverged yeast populations
It is found that subtelomeric regions play a key role in defining individual quantitative variation, emphasizing the importance of the adaptive nature of these regions in natural populations.
The results reported here cannot be explained by the classical hypothesis of reduction in the number of loci segregating for traits with greater impact on fitness and confirm that traits with more impact on Fitness are more strongly canalized.