Characterization of thePristionchus pacificus“epigenetic toolkit” reveals the evolutionary loss of the histone methyltransferase complex PRC2

Abstract

Comparative approaches have revealed both divergent and convergent paths to achieving shared developmental outcomes. Thus, only through assembling multiple case studies can we understand biological principles. Yet, despite appreciating the conservation – or lack thereof – of developmental networks, the conservation of epigenetic mechanisms regulating these networks is poorly understood. The nematodePristionchus pacificushas emerged as a model system of plasticity and epigenetic regulation as it exhibits a bacterivorous or omnivorous morph depending on its environment. Here, we determined the “epigenetic toolkit” available toP. pacificusas a resource for future functional work on plasticity, and as a comparison withC. elegansto investigate the conservation of epigenetic mechanisms. Broadly, we observed a similar cast of genes with putative epigenetic function betweenC. elegansandP. pacificus. However, we also found striking differences. Most notably, the histone methyltransferase complex PRC2 appears to be missing inP. pacificus.We described the deletion/pseudogenization of the PRC2 genesmes-2andmes-6and concluded that both were lost in the last common ancestor ofP. pacificusand a related speciesP. arcanus.Interestingly, we observed the enzymatic product of PRC2 (H3K27me3) by mass spectrometry and immunofluorescence, suggesting that a currently unknown methyltransferase has been co-opted for heterochromatin silencing. Altogether, we have provided an inventory of epigenetic genes inP. pacificusto enable reverse-genetic experiments related to plasticity, and in doing so have described the first loss of PRC2 in a multicellular organism.