ArticlePLoS genetics2023
Characterization of factors that underlie transcriptional silencing in C. elegans oocytes.
Article in PLoS genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- RNA Pol I shapes meiotic chromatin, germline H3K4me3 dynamics, and oogenesis independent of ribosome assembly.Cell reports · 2026Article
- RNA Pol I activity is required for meiotic chromatin organization and the H3K4me3 gradient essential for oogenesis, independent of ribosome synthesis.bioRxiv : the preprint server for biology · 2025Article
- FG repeats drive co-clustering of nuclear pores and P granules in the C. elegans germline.Development (Cambridge, England) · 2025Article
- Article
- Nuclear Argonaute protein NRDE-3 switches small RNA partners during embryogenesis to mediate temporal-specific gene regulatory activity.bioRxiv : the preprint server for biology · 2025Article
- The TOP-2/condensin II axis silences transcription during germline specification in C. elegans.G3 (Bethesda, Md.) · 2024Article
- Transcriptional repression during spermatogenesis inmicroPublication biology · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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.
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