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However, its role in spermatogenesis remains elusive. Here, we demonstrate an essential role of Ash2l for meiotic prophase but dispensable for mitosis in differentiated spermatogonia. Using a germ cell-specific Ash2l knockout mouse model, we reveal that Ash2l deficiency leads to meiotic arrest and sterility in both sexes. Ash2l-deficient spermatocytes exhibit failures in chromosomal synapsis associated with persistent DMC1 foci and \u03b3H2AX, resulting in meiocyte loss due to apoptosis. Conversely, Ash2l-deficient differentiated spermatogonia show normal development. Mechanistically, Ash2l deficiency results in a global loss of H3K4me3 in promoter regions and significantly decreases expression of thousands of genes. Among these are genes involved in epigenetic silencing pathways, such as H3K9 di-methylation, DNA methylation and piRNA pathways, that are crucial for transposon repression during meiotic prophase I progression. Supporting this, we observe that Ash2l mutant spermatocytes display ectopic expression of LINE1-ORF1P. Our findings therefore reveal the previously unappreciated role of ASH2L-dependent H3K4me3 modification in spermatogenesis and provide clues to the molecular mechanisms in epigenetic disorders underlying male infertility.<\/jats:p>","DOI":"10.1242\/dev.204630","type":"journal-article","created":{"date-parts":[[2025,2,24]],"date-time":"2025-02-24T14:05:23Z","timestamp":1740405923000},"source":"Crossref","is-referenced-by-count":3,"title":["The KMT2 complex protein ASH2L is required for meiotic prophase progression but dispensable for mitosis in differentiated spermatogonia"],"prefix":"10.1242","volume":"152","author":[{"given":"Zhen","family":"Lin","sequence":"first","affiliation":[{"name":"Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, University of Chinese Academy of Sciences, Chinese Academy of Sciences 1 Key Laboratory of Multi-Cell System, Shanghai Key Laboratory of Molecular Andrology , , Shanghai 200031 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