404V Poster Online - Virtual Posters
Tuesday June 07, 11:00 AM - 3:00 PM

Authors:
Abigail DiVito Evans ^1,2; Regina Fairbanks ³; Paul Schmidt ¹; Mia Levine ^1,2

Affiliations:
1) Department of Biology, University of Pennsylvania, Philadelphia, PA; 2) Epigenetics Institute, University of Pennsylvania, Philadelphia, PA; 3) Department of Evolution and Ecology, University of California, Davis, Davis, CA

Keywords:
Genetic interactions

Spatially- and temporally-varying selection can shape variation of heritable phenotypes across geographic space and seasonal time. Many such phenotypes exhibit genotype-dependent plastic responses to the environment (genotype-by-environment interaction, “GxE”). Building evidence suggests genotype-specific gene expression programs mediate observed patterns of GxE. However, the mechanisms that determine this gene expression variation, and ultimately phenotypic variation, remain poorly described. Genomic DNA complexed with specialized packaging proteins (i.e. chromatin) is a classic, environment-sensitive determinant of gene expression. Surprisingly, few studies have addressed the role of chromatin in mediating GxE. To fill this gap, we exploit an environment-sensitive phenotype that varies across both geographic space and seasonal time in a tractable model system. Drosophila melanogaster, in response to the cold temperatures and short days of oncoming winter, enters reproductive arrest, called diapause. Diapause is a complex trait characterized by extensive physiological changes that result in suspended egg production. In inbred D. melanogaster strains that lack genetic variation, only a portion of individuals in the same environment enter diapause. This phenotypic variation in the absence of genetic variation is a classic signature of chromatin-based epigenetic regulation, and allows us to compare diapausing ovaries and reproductive ovaries under the same environmental conditions. To identify how chromatin mediates genotype-dependent diapause incidence, we exploit two inbred lines that span the spectrum of diapause incidence in response to simulated winter conditions: a high diapause (HD) line with 90% diapause incidence and a low diapause (LD) line with 5% diapause incidence. We discovered that silent histone marks H3K27me3 and H3K9me3, and active mark H3K36me1, are invariant across HD and LD ovaries. In contrast, the active histone mark H3K4me3 is depleted in HD diapausing ovaries while active marks H3K27ac and H3K9ac are depleted in LD reproductive ovaries. This genotype-dependent histone mark abundance implicates genotype-specific gene regulation. Consistent with this hypothesis, gene expression in diapausing ovaries only partially overlaps across genotypes. To determine if genotype-specific histone marks are causally linked to diapause incidence, we used ovary-specific RNAi to deplete histone mark “writer” and “eraser” enzymes. Depleting H3K4me3 increases diapause incidence in both lines and enriching H3K4me3 decreases diapause incidence in the HD line only. Moreover, decreasing H3K9me3 and H3K36me3 in the LD line increases diapause incidence, but has no effect on the HD line. This study is the first to reveal a causal role of chromatin-based, epigenetic regulation in mediating an adaptive, genotype-dependent response to the environment.