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R-loop maintains the deposition of H3K36me3 to prevent invasion of H3K4me3 during SN-oocyte development [3]

ABSTRACT: Establishment of epigenetic modifications in an orderly manner is crucial for oocyte maturation and embryonic development. R-loop (DNA/RNA hybrids) plays an important role in regulating genome stability, epigenetic modifications and gene expression. However, the specific functions and regulatory mechanisms of R-loop on the crosstalk between histone modifications during oocyte development remain unclear. Here, we find that loss of R-loop by overexpressing Rnaseh1 significantly slow down oocyte development. R-loop loss in germinal vesicle (GV) oocyte leads to downregulation of H3K36me3 at key oocyte developmental gene bodies, aberrant invasion of H3K4me3 into H3K36me3-marked regions, resulting in dysregulated gene expression and ultimately hindering oocyte development. Importantly, this dysregulated gene expression can be rescued by histone H3K36me3 methyltransferase SETD2 targeting on specific R-loop-dependent H3K36me3-marked regions. Together, this finding reveals that R-loop acts as a crucial regulator in controlling epigenetic crosstalk of H3K36me3 and H3K4me3 in maternal genome, ensuring normal oocyte development.

ORGANISM(S): Mus musculus

PROVIDER: GSE285237 | GEO | 2026/07/13

REPOSITORIES: GEO

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Project description:Epithelial to mesenchymal transition (EMT) is an extreme example of cell plasticity, important for normal development, injury repair, and malignant progression. Widespread epigenetic reprogramming occurs during stem cell differentiation and malignant transformation, but EMT-related epigenetic reprogramming is poorly understood. Here we investigated epigenetic modifications during TGF-β-mediated EMT. While DNA methylation was unchanged during EMT, we found global reduction of the heterochromatin mark H3-lys9 dimethylation (H3K9Me2), increase of the euchromatin mark H3-lys4 trimethylation (H3K4Me3), and increase of the transcriptional mark H3-lys36 trimethylation (H3K36Me3). These changes were largely dependent on lysine-specific deaminase-1 (LSD1), and LSD1 loss-of-function experiments showed marked effects on EMT-driven cell migration and chemoresistance. Genome-scale mapping revealed that chromatin changes were largely specific to large organized heterochromatin K9-modifications (LOCKs), suggesting that EMT is characterized by reprogramming of specific chromatin domains across the genome. Chromatin immunoprecipitation (ChIP) was performed with antibodies against H3K9Me2 (Abcam, ab1220), H3K36Me3 (ab9050), and H3K4Me3 (ab8580) on native (unfixed) chromatin isolated from fully differentiated mouse AML12 cells (confluent, serum starved for 48hrs) either treated with TGF-β for 36hrs to induce EMT or not treated with TGF-β (0hrs, differentiated AML12 cells). DNA purified from these samples was then either whole-genome amplified (H3K36Me3 and H3K4Me3) and hybridized or directly (H3K9Me2) hybridized to NimbleGen 2.1M economy whole-genome tiling arrays #2 (listed below as array 1) and #3 (listed below as array 2), which cover mouse chromosomes 4-14. For each sample, the immunoprecipitated DNA (IP) and the input (control) DNA were hybridized to the arrays, and the IP is normalized to the input. There are 16 total samples listed below. There are 8 sample for H3K9Me2 (TGF-β and no TGF-β for arrays 1 and 2, done in replicate for a total of 8). There are 4 samples for H3K36Me3 (TGF-β and no TGF-β done on array 1 and array 2). There are 4 total samples for H3K4Me3 (TGF-β and no TGF-β done on array 1 and array 2).

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R-loop maintains the deposition of H3K36me3 to prevent invasion of H3K4me3 during SN-oocyte development [3]

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