Nematodes adapt using yin-yang isoforms of a NURF subunit

Abstract

Convergent or parallel evolution is the repeated evolution of the same genotype in independent populations in response to similar environmental changes. A growing number of examples of parallel evolution are accumulating in the literature (e.g. cis-regulatory changes in the shavenbaby developmental regulator in Drosophila species result in dorsal cuticle hair loss [1], repeated selection on the Eda TNF ligand causes stickleback low-plated phenotype [2], and deletion of chemoreceptor genes contribute to the insensitivity to a specific pheromone in Caenorhabditis species [3]). In this dissertation, I discussed my studies of how Caenorhabditis elegans strains adapt to laboratory environments. I described how two C. elegans strains N2 and LSJ2, who share a common ancestor but have evolved independently in laboratory conditions have increased fitness in their respective environment. I showed that part of adaptation in the LSJ2 strain is caused by a 60 bp deletion in nurf-1 gene, a subunit of nucleosome remodeling factor NURF. Next, I described my finding about that adaptation of the N2 lineage is partially caused by a SNV (single nucleotide variation) in the 2nd intron of nurf-1. This work suggests that nurf-1 is a common target of evolution in response to laboratory growth. Finally, I described my work to understand why nurf-1 might be targeted, which I propose is due to the antagonistic function (here I refer as Yin-yang) of two major nurf-1 isoforms on the sexual fate during gametogenesis. My doctoral thesis study advances our understanding of how nucleosome remodeling factor may work and that isoform-level study of complex genes is feasible and necessary.