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Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse [RNA-seq]

ABSTRACT: RNA-seq on spermatogenic cells from P12 testes

ORGANISM(S): Mus musculus

PROVIDER: GSE119178 | GEO | 2019/05/09

REPOSITORIES: GEO

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Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse [ATAC-seq]

Project description:ATAC-seq on spermatogenic cells from P12 and P18 testes

2019-05-09 | GSE119176 | GEO

Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse [ChIP-seq]

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Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse [CUT&RUN]

Project description:CUT&RUN to monitor SCML2 localization in BRG1-WT and BRG1-cKO spermatogenic cells

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Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate male germline transcription in the mouse.

Project description:A deficiency in BRG1, the catalytic subunit of the SWI/SNF chromatin remodeling complex, results in a meiotic arrest during spermatogenesis. Here, we explore the causative mechanisms. BRG1 is preferentially enriched at active promoters of genes essential for spermatogonial pluripotency and meiosis. In contrast, BRG1 is also associated with the repression of somatic genes. Chromatin accessibility at these target promoters is dependent upon BRG1. These results favor a model in which BRG1 coordinates spermatogenic transcription to ensure meiotic progression. In spermatocytes, BRG1 interacts with SCML2, a testis-specific PRC1 factor that is associated with the repression of somatic genes. We present evidence to suggest that BRG1 and SCML2 concordantly regulate genes during meiosis. Furthermore, BRG1 is required for the proper localization of SCML2 and its associated deubiquitylase, USP7, to the sex chromosomes during pachynema. SCML2-associated mono-ubiquitylation of histone H2A lysine 119 (H2AK119ub1) and acetylation of histone lysine 27 (H3K27ac) are elevated in Brg1cKO testes. Coincidentally, the PRC1 ubiquitin ligase RNF2 is activated while a histone H2A/H2B deubiquitylase USP3 is repressed. Thus, BRG1 impacts the male epigenome by influencing the localization and expression of epigenetic modifiers. This mechanism highlights a novel paradigm of cooperativity between SWI/SNF and PRC1.

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Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-05-09 | GSE119179 | GEO

Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse

Project description:Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse

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Epigenetic antagonism between polycomb and SWI/SNF complexes during oncogenic transformation.

Project description:Epigenetic alterations have been increasingly implicated in oncogenesis. Analysis of Drosophila mutants suggests that Polycomb and SWI/SNF complexes can serve antagonistic developmental roles. However, the relevance of this relationship to human disease is unclear. Here, we have investigated functional relationships between these epigenetic regulators in oncogenic transformation. Mechanistically, we show that loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2 and that Polycomb targets are broadly H3K27-trimethylated and repressed in SNF5-deficient fibroblasts and cancers. Further, we show antagonism between SNF5 and EZH2 in the regulation of stem cell-associated programs and that Snf5 loss activates those programs. Finally, using conditional mouse models, we show that inactivation of Ezh2 blocks tumor formation driven by Snf5 loss.

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Transcriptional Metabolic Reprograming Drives Meiotic Fate Decision in Mammalian Germ Cells

Project description:Nitrogen starvation drives meiosis in yeasts1, while retinoic acid (RA) is required for mammalian meiosis through the activation of its germline-specific target, stimulated by retinoic acid gene 8 (Stra8).Here, by using single-cell transcriptome analysis of wild-type and Stra8-deficient testes, our data revealed that the expression of major metabolic genes are downregulated during germ cell entry into meiosis. Recently, we collected mouse testicular cells from wild-type and Stra8-deficient mice at postnatal day 12 (P12) and P21 for single cell RNA-sequencing (scRNA-seq). Upon scRNA-seq, we obtained a total of 23,470 cells from these samples. Using stringent quality control, 22,839 cells were selected for further analysis. All cells, including both wild-type and Stra8-deficient testicular cells, were pooled together to perform clustering analysis, which revealed 6 major cell clusters based on their distinct gene expression patterns. We annotated these six clusters by using known marker genes, including spermatogonia (SPG; Stra8; 3,941 cells), spermatocyte (SPC; Syce1; 4,924 cells), spermatid (STD; Acrv1; 710 cells), Sertoli cell (SC; Sox9; 9,488 cells), Myeloid (MYD; Acta2; 3,531 cells), and Leydig Cells (LY; Star; 245 cells). There is an increase in the percentage of spermatogonia in Stra8-deficient testes at both P12 (28% versus 14% in wild-type) and P21 (17% versus 10% in wild-type). At P21, while spermatocytes are abundant and spermatid are formed in wild-type testes, there are only a few spermatocytes (0.2% versus 73% in wild-type), and spermatids are absent in Stra8-deficient testes. Signature genes are enriched for GO terms for distinct biological function and metabolic pathways in different cell types.

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Mammalian SWI/SNF complexes in cancer: emerging therapeutic opportunities.

Project description:Mammalian SWI/SNF (BAF) chromatin remodeling complexes orchestrate a diverse set of chromatin alterations which impact transcriptional output. Recent whole-exome sequencing efforts have revealed that the genes encoding subunits of mSWI/SNF complexes are mutated in over 20% of cancers, spanning a wide range of tissue types. The majority of mutations result in loss of subunit protein expression, implicating mSWI/SNF subunits as tumor suppressors. mSWI/SNF-deficient cancers remain a therapeutic challenge, owing to a lack of potent and selective agents which target complexes or unique pathway dependencies generated by mSWI/SNF subunit perturbations. Here, we review the current landscape of mechanistic insights and emerging therapeutic opportunities for human malignancies driven by mSWI/SNF complex perturbation.

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Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse [ATAC-seq]

Project description:Mammalian SWI/SNF collaborates with a polycomb-associated protein to regulate germ line transcription in the mouse [ATAC-seq]

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