Presentation/Session Information

Session Information

Session Title: Cell Fate, Differentiation and Morphogenesis Session Type: Parallel
Session Location: Northwest Auditorium Session Time: Sat, Jun 27 8:30AM - 11:30AM

Presentation Information

Program Number: 189 Presentation Time: 11:18AM - 11:30AM

Presentation Content

Regulation of embryonic genome activation by endoRNAi.Christina Fassnacht, Cristina Tocchini, Jorge Merlet, Michael Stadler, Rafal Ciosk. Epigenetics, Friedrich Miescher Institute, Bas

In order to give rise to a new organism, cells in the early embryo must be developmentally flexible. This developmental plasticity, or pluripotency, is acquired during the so-called oocyte-to-embryo transition, when a terminally differentiated oocyte is reprogrammed into an undifferentiated embryo. The precise regulation of reprogramming is critical, since germ cells that precociously acquire pluripotency can develop into germ cell tumors, called teratomas. To understand the mechanisms controlling oocyte reprogramming we performed a genetic screen, looking for mutants in which embryonic genome activation (EGA), a marker for pluripotency, occurs precociously in germ cells. One regulator of pluripotency identified in this screen is the TRIM-NHL protein LIN-41, which prevents a premature onset of embryonic-like differentiation in developing oocytes (Tocchini et al., 2014). In addition to lin-41, our screen identified a distinct class of mutants, in which the developing oocytes prematurely induce embryonic genome activation but do not differentiate further into teratomas. Additionally, in these mutants, EGA occurs without reactivating the cell cycle, which accompanies EGA in lin-41 mutants, suggesting that the corresponding genes may be controlling transcriptional reprogramming more directly. We mapped the mutants to core components of the RNA-dependent RNA polymerase (RdRP) complex, which synthesizes secondary siRNAs, called 22G RNAs. The two major endoRNAi pathways are the WAGO (worm-specific Argonaute) and the CSR-1 (chromosome-segregation and RNAi-deficient-1) pathway. Further analysis revealed that it is the CSR-1 pathway that inhibits EGA in developing oocytes, since mutants in the CSR-1 pathway show EGA, whereas in the WAGO pathway they do not. We suggest that this function of CSR-1 is 22G RNA-dependent, as for example, interfering with 22G RNA levels by depleting CDE-1 (cosuppression defective-1) similarly leads to precious EGA. So far, the CSR-1 pathway has been only shown to promote germline gene expression, whereas our findings suggest a new and intriguing inhibitory role for this pathway in reprogramming transcription during the oocyte-to-embryo transition.

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