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Epigenetic mechanisms of nematode mouth-form plasticity


Werner,  M       
Department Integrative Evolutionary Biology, Max Planck Institute for Developmental Biology, Max Planck Society;

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Werner, M. (2018). Epigenetic mechanisms of nematode mouth-form plasticity. Poster presented at EMBO Workshop: C. Elegans Development, Cell Biology and Gene Expression, | Barcelona, Spain.

Cite as: https://hdl.handle.net/21.11116/0000-000B-4158-9
Self-recognition is observed abundantly throughout the natural world regulating diverse biological processes. Although ubiquitous, often little is known about the associated molecular mechanisms and despite the prevalence of nematodes in nearly every ecological niche and the pre-eminence of Caenorhabditis elegans as a model organism, evidence of self-recognition has thus far never been dMany animals and plants can respond to their environment by developmental plasticity, the ability to produce different phenotypes form the same genotype. In nematodes crowding and starvation regulate entry into an arrested dauer stage, and in some species an alternative mouth-form decision (bacterivorous vs. predatory). While forward genetic screens have elucidated many of responsible genes, the epigenetic mechanisms connecting the environment to these gene-switches is still lacking. We used the mouth form plasticity of Pristionchus pacificus as model to understand the molecular mechanisms of environmental influence. First, we established a set of culture conditions to easily tune bacterivorous vs. predatory mouth forms, and then performed RNA-seq at every major developmental stage in conditions that induce either mouth form. We have identified the identity and timing of large gene networks corresponding to each mouth form. We also performed temporal morphometric analysis to determine when the phenotypic decision is made. By combining these data with reciprocal transplant experiments, we identified a ~36 hr critical window between juvenile stage 2 and 4 in which the mouth form phenotype is susceptible to the environment. Finally, we profiled dynamic chromatin changes by ChIP-seq and ATAC-seq before, during, and after this critical window in bacterivorous and predatory-inducing conditions. Collectively, our results reveal changes in the chromatin landscape associated with environmental switches, and insight into the molecular mechanisms of phenotypic plasticity.