Characterization of factors that underlie transcriptional silencing in C. elegans oocytes.

Autor: Belew MD; Department of Biological Sciences, Molecular and Computational Biology Section, University of Southern California, Los Angeles, California, United States of America., Chien E; Department of Biological Sciences, Molecular and Computational Biology Section, University of Southern California, Los Angeles, California, United States of America., Michael WM; Department of Biological Sciences, Molecular and Computational Biology Section, University of Southern California, Los Angeles, California, United States of America.
Jazyk: angličtina
Zdroj: PLoS genetics [PLoS Genet] 2023 Jul 21; Vol. 19 (7), pp. e1010831. Date of Electronic Publication: 2023 Jul 21 (Print Publication: 2023).
DOI: 10.1371/journal.pgen.1010831
Abstrakt: While it has been appreciated for decades that prophase-arrested oocytes are transcriptionally silenced on a global level, the molecular pathways that promote silencing have remained elusive. Previous work in C. elegans has shown that both topoisomerase II (TOP-2) and condensin II collaborate with the H3K9me heterochromatin pathway to silence gene expression in the germline during L1 starvation, and that the PIE-1 protein silences the genome in the P-lineage of early embryos. Here, we show that all three of these silencing systems, TOP-2/condensin II, H3K9me, and PIE-1, are required for transcriptional repression in oocytes. We find that H3K9me3 marks increase dramatically on chromatin during silencing, and that silencing is under cell cycle control. We also find that PIE-1 localizes to the nucleolus just prior to silencing, and that nucleolar dissolution during silencing is dependent on TOP-2/condensin II. Our data identify both the molecular components and the trigger for genome silencing in oocytes and establish a link between PIE-1 nucleolar residency and its ability to repress transcription.
Competing Interests: The authors declare no competing interests.
(Copyright: © 2023 Belew et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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