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Abstract
Sexual reproduction involves the creation of sex-dependent gametes, oocytes and sperm. In mammals, sexually dimorphic differentiation commences in the primordial germ cells (PGCs) in embryonic gonads; PGCs in ovaries and testes differentiate into meiotic primary oocytes and mitotically quiescent prospermatogonia, respectively. Here, we show that the transition from PGCs to sex-specific germ cells was abrogated in conditional knockout mice carrying a null mutation of Smarcb1 (also known as Snf5) gene, which encodes a core subunit of the SWI/SNF chromatin remodeling complex. In female mutant mice, failure to upregulate meiosis-related genes resulted in impaired meiotic entry and progression, including defects in synapsis formation and DNA double strand break repair. Mutant male mice exhibited delayed mitotic arrest and DNA hypomethylation in retrotransposons and imprinted genes, resulting from aberrant expression of genes related to growth and de novo DNA methylation. Collectively, our results demonstrate that the SWI/SNF complex is required for transcriptional reprogramming in the initiation of sex-dependent differentiation of germ cells.
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Details
1 Kitasato University, Laboratory of Stem Cell Biology, Graduate School of Science, Department of Biosciences, School of Science, Sagamihara, Japan (GRID:grid.410786.c) (ISNI:0000 0000 9206 2938)
2 Yokohama City University Graduate School of Medicine, Department of Immunology, Yokohama, Japan (GRID:grid.268441.d) (ISNI:0000 0001 1033 6139)
3 Josai International University, Faculty of Pharmaceutical Sciences, Togane, Japan (GRID:grid.440885.5) (ISNI:0000 0000 9365 1742)