ArticleiScience2025
MGA directly recruits SETDB1/ATF7IP for histone H3K9me3 mark on meiosis-related genes in mouse embryonic stem cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- The Many Faces of SetDB1.Epigenomes · 2026Review
- Epigenetic relay: Polycomb-directed DNA methylation in mammalian development.PLoS genetics · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycomb repressive complex 1.6 (PRC1.6), one of the PRC1 subtypes, plays crucial roles in preventing the ectopic expression of meiosis-related genes in mouse embryonic stem cells (ESCs). In addition to the histone modifications H2AK119ub1 and H3K27me3 that are deposited by PRC1 and PRC2, respectively, many meiosis-related genes bear the trimethylated lysine 9 of histone H3 (H3K9me3) mark in ESCs. However, the precise molecular mechanisms that deposit this mark on these genes in ESCs remain unknown. Here, we demonstrated that MGA, a scaffolding component of PRC1.6, is directly involved in recruiting SETDB1, an enzyme that catalyzes this histone modification, via its interaction with ATF7IP. Thus, our findings indicate that MGA plays a dual role, first being central in establishing a PRC1/PRC2-dependent repressive state by contributing to the construction of PRC1.6 as a scaffolding component, and then inducing a more robustly repressed state by recruiting the STEDB1/ATF7IP complex for H3K9me3 modification.
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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 Socratic graph.