Submission Type
Poster
Abstract
Polyphenism, the ability of an organism to produce discrete alternative phenotypes in response to environmental conditions, exemplifies the non-linear relationship among genes, the traits they influence, and the environment. While several genes that regulate polyphenism have been identified in some systems, such as the nematode Pristionchus pacificus, which exhibits a resource polyphenism in the development of alternative mouth morphologies, it is generally unknown which loci harbor intraspecific variation for polyphenism. Quantitative traits, consisting of many genes and their interactions with the environment, are expected to harbor variation, even among individuals with the same ultimate phenotype. As a first approach to identify epistatic or additive interactions underlying variation in polyphenic responses, we performed crosses between lineages with similar phenotypes, thereafter isolating progeny that display phenotypes outside the range of the parentals. We then created a panel of recombinant inbred lines including parental and transgressive phenotypes, followed by quantitative trait locus mapping of recombinant offspring displaying extreme phenotypes. Identification of candidate, causal loci will be followed by functional validation using allelic replacements as mediated by CRISPR/Cas 9 gene editing, according to established techniques in the P. pacificus system. In summary, this work harnesses naturally occurring variation among lineages to inform how the genetic architecture of a polyphenism evolves.
Included in
Uncovering Natural Variation in the Mechanisms of a Polyphenism
Polyphenism, the ability of an organism to produce discrete alternative phenotypes in response to environmental conditions, exemplifies the non-linear relationship among genes, the traits they influence, and the environment. While several genes that regulate polyphenism have been identified in some systems, such as the nematode Pristionchus pacificus, which exhibits a resource polyphenism in the development of alternative mouth morphologies, it is generally unknown which loci harbor intraspecific variation for polyphenism. Quantitative traits, consisting of many genes and their interactions with the environment, are expected to harbor variation, even among individuals with the same ultimate phenotype. As a first approach to identify epistatic or additive interactions underlying variation in polyphenic responses, we performed crosses between lineages with similar phenotypes, thereafter isolating progeny that display phenotypes outside the range of the parentals. We then created a panel of recombinant inbred lines including parental and transgressive phenotypes, followed by quantitative trait locus mapping of recombinant offspring displaying extreme phenotypes. Identification of candidate, causal loci will be followed by functional validation using allelic replacements as mediated by CRISPR/Cas 9 gene editing, according to established techniques in the P. pacificus system. In summary, this work harnesses naturally occurring variation among lineages to inform how the genetic architecture of a polyphenism evolves.
