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H2A.Z reinforces maternal H3K4me3 formation and is essential for meiotic progression in mouse oocytes [RNA-Seq]

GSE262049 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2025/03/01 Platform GPL30172Platform GPL19057
Summary
Mammalian oocytes establish a unique landscape of histone modifications, some of which are inherited by early embryos. How histone variants shape the maternal histone landscape remains unknown. Here, we map histone H2A variants in mouse fully grown oocytes (FGOs) and find that H2A.Z forms broad domains across intergenic regions, along non-canonical H3K4me3 (ncH3K4me3). During oocyte growth, H2A.Z progressively transitions from an active promoter-rich, canonical distribution to a non-canonical broad distribution (ncH2A.Z). Depletion of H2A.Z in oocytes partially impairs ncH3K4me3 formation and causes severe defects in meiotic progression, which resemble Mll2-knockout oocytes. Conversely, depletion of ncH3K4me3 by Mll2 knockout also causes a reduction of ncH2A.Z in FGOs. Thus, our study suggests that ncH2A.Z and ncH3K4me3 reinforce each other to form functional oocytes.
Published in
H2A.Z reinforces maternal H3K4me3 formation and is essential for meiotic progression in mouse oocytes
Mei H, Hayashi R, Kozuka C et al. · Nature structural & molecular biology 2025 · PMID 40514539 · doi:10.1038/s41594-025-01573-x
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Also filed as BioProject PRJNA1090094 and SRA study SRP496727. Searching any of these in the dataset finder brings you back here.

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