The CSR-1 endogenous RNAi pathway ensures accurate transcriptional reprogramming during the oocyte-to-embryo transition in Caenorhabditis elegans

PLoS Genet. 2018 Mar 26;14(3):e1007252. doi: 10.1371/journal.pgen.1007252. eCollection 2018 Mar.

Abstract

Endogenous RNAi (endoRNAi) is a conserved mechanism for fine-tuning gene expression. In the nematode Caenorhabditis elegans, several endoRNAi pathways are required for the successful development of reproductive cells. The CSR-1 endoRNAi pathway promotes germ cell development, primarily by facilitating the expression of germline genes. In this study, we report a novel function for the CSR-1 pathway in preventing premature activation of embryonic transcription in the developing oocytes, which is accompanied by a general Pol II activation. This CSR-1 function requires its RNase activity, suggesting that, by controlling the levels of maternal mRNAs, CSR-1-dependent endoRNAi contributes to an orderly reprogramming of transcription during the oocyte-to-embryo transition.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Genetically Modified
  • Caenorhabditis elegans / embryology*
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans Proteins / genetics*
  • Caenorhabditis elegans Proteins / metabolism
  • Embryo, Nonmammalian
  • Female
  • Gene Expression Regulation, Developmental
  • Mutation
  • Oocytes / physiology*
  • RNA Interference*
  • RNA Polymerase II / genetics
  • RNA Polymerase II / metabolism
  • Transcription Factors / genetics

Substances

  • CSR-1 protein, C elegans
  • Caenorhabditis elegans Proteins
  • GLD-1 protein, C elegans
  • LIN-41 protein, C elegans
  • Transcription Factors
  • RNA Polymerase II

Grants and funding

This work was supported by the Swiss National Science Foundation (http://www.snf.ch/en/Pages/default.aspx) through the grant 31003A_149402, by the National Science Centre Poland (https://www.ncn.gov.pl/) through the grant 2015/19/B/NZ3/02412 and by an EMBO Installation Grant (http://www.embo.org/funding-awards/installation-grants) to RC. PK has received funding for the research leading to these results from the EMBO Fellowship (http://www.embo.org/, ALTF 95-2015). The Friedrich Miescher Institute for Biomedical Research is sponsored by the Novartis Research Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.