ArticleProceedings of the National Academy of Sciences of the United States of America2024
Morc1 reestablishes H3K9me3 heterochromatin on piRNA-targeted transposons in gonocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- MORC1 coordinates TRIM28 interaction and nuclear condensate formation for transposon silencing.iScience · 2026Article
- Transposable element regulation in mammalian germ cells and other contexts: multilayered repression, fertility, and regulated activation.Epigenomics · 2026Review
- Landscape and biogenesis of piRNAs in HBV-associated hepatocarcinogenesis: from repetitive elements to oncogenic circuits.Discover oncology · 2026Review
- Beyond silencing: integrative multi-omics and spatial profiling unravel the systems-level role of piRNAs in HBV-driven Hepatocarcinogenesis.Molecular biology reports · 2026Review
- Report on the seventh Japanese meeting on biological function and evolution through interactions between hosts and transposable elements.Mobile DNA · 2026Article
- Ancestral pattern of theProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Gonocytes in Transition: Establishing the Male Germline Identity.Advances in experimental medicine and biology · 2026Review
- Stage-dependent dual mechanisms of MORC2 in retrotransposon silencing and sex chromosome inactivation in germ cells.Nucleic acids research · 2025Article
- Early female germline development inProceedings of the National Academy of Sciences of the United States of America · 2025Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
To maintain fertility, male mice re-repress transposable elements (TEs) that were de-silenced in the early gonocytes before their differentiation into spermatogonia. However, the mechanism of TE silencing re-establishment remains unknown. Here, we found that the DNA-binding protein Morc1, in cooperation with the methyltransferase SetDB1, deposits the repressive histone mark H3K9me3 on a large fraction of activated TEs, leading to heterochromatin. Morc1 also triggers DNA methylation, but TEs targeted by Morc1-driven DNA methylation only slightly overlapped with those repressed by Morc1/SetDB1-dependent heterochromatin formation, suggesting that Morc1 silences TEs in two different manners. In contrast, TEs regulated by Morc1 and Miwi2, the nuclear PIWI-family protein, almost overlapped. Miwi2 binds to PIWI-interacting RNAs (piRNAs) that base-pair with TE mRNAs via sequence complementarity, while Morc1 DNA binding is not sequence specific, suggesting that Miwi2 selects its targets, and then, Morc1 acts to repress them with cofactors. A high-ordered mechanism of TE repression in gonocytes has been identified.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.