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.
Highlights
We demonstrate that a specific endoRNAi pathway, employing the Argonaute protein CSR-1, functions as a break on gene-specific, and potentially global, activation of embryonic transcription in the developing oocytes
Our observations suggest a model, where CSR-1–dependent titration of maternal mRNAs is required to delay the onset of embryonic transcription until its physiological onset in early embryos
During the oocyte-to-embryo transition, the RNA binding proteins (RBPs) GLD-1 and LIN-41 inhibit the onset of embryonic transcription in oogenic germ cells [4, 5]
Summary
Developmental plasticity, or pluripotency, is acquired during the oocyte-to-embryo transition, during which a highly specialized cell, the oocyte, is reprogrammed into a developmentally. A small RNA pathway helps control the transition between generations 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 funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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