ArticleNucleic acids research2021
HDAC3 controls male fertility through enzyme-independent transcriptional regulation at the meiotic exit of spermatogenesis.
Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- miR-132-y TargetsBiomolecules · 2026Article
- Histone deacetylase enzyme activity is not the universal anticancer target of HDAC inhibitors.Signal transduction and targeted therapy · 2026Article
- Chronic high-fat diet decreases global histone H4 acetylation and increases HDAC8 expression in mouse testes.Biochemistry and biophysics reports · 2026Article
- Decoding Infertility: the Epigenetic Influence of HDACs on Reproductive Function.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Gut Microbial Dysbiosis and Male Reproductive Health: Current Insights and Future Directions.International journal of molecular sciences · 2026Review
- Male germ cell-specific deletion ofZoological research · 2026Article
- HDAC3 Preserves the primordial follicle reserve by epigenetically suppressing ferroptosis in pregranulosa cells.Cellular and molecular life sciences : CMLS · 2026Article
- Epigenetic regulation by DNA methylation, histone modifications and chromatin remodeling complexes in controlling spermatogenesis and their dysfunction with male infertility.Cellular and molecular life sciences : CMLS · 2025Review
- Enzyme-independent functions of HDAC3 in the adult heart.Acta pharmaceutica Sinica. B · 2025Article
- Adverse Effects of Nicotine on Human Sperm Nuclear Proteins.The world journal of men's health · 2025Review
- Perfluorohexane Sulfonic Acid Disrupts the Immune Microenvironment for Spermatogenesis by Damaging the Structure of the Blood-Testis Barrier in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NKAPL facilitates transcription pause-release and bridges elongation to initiation during meiosis exit.Nature communications · 2025Article
- Generation and analysis of a mouse multitissue genome annotation atlas.Genome research · 2024Article
- DCAF2 regulates the proliferation and differentiation of mouse progenitor spermatogonia by targeting p21 and thymine DNA glycosylase.Cell proliferation · 2024Article
- Unfolding the complexity of epigenetics in male reproductive aging: a review of therapeutic implications.Molecular biology reports · 2024Review
- Article
- Generation and analysis of a mouse multi-tissue genome annotation atlas.bioRxiv : the preprint server for biology · 2024Article
- Separation of transcriptional repressor and activator functions in Drosophila HDAC3.Development (Cambridge, England) · 2023Article
- Loss of PMFBP1 Disturbs Mouse Spermatogenesis by Downregulating HDAC3 Expression.Journal of assisted reproduction and genetics · 2023Article
Corrections and comments
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Authors and funding
27 authors at 6 institutions in 2 countries.
Funding
Abstract
The transition from meiotic spermatocytes to postmeiotic haploid germ cells constitutes an essential step in spermatogenesis. The epigenomic regulatory mechanisms underlying this transition remain unclear. Here, we find a prominent transcriptomic switch from the late spermatocytes to the early round spermatids during the meiotic-to-postmeiotic transition, which is associated with robust histone acetylation changes across the genome. Among histone deacetylases (HDACs) and acetyltransferases, we find that HDAC3 is selectively expressed in the late meiotic and early haploid stages. Three independent mouse lines with the testis-specific knockout of HDAC3 show infertility and defects in meiotic exit with an arrest at the late stage of meiosis or early stage of round spermatids. Stage-specific RNA-seq and histone acetylation ChIP-seq analyses reveal that HDAC3 represses meiotic/spermatogonial genes and activates postmeiotic haploid gene programs during meiotic exit, with associated histone acetylation alterations. Unexpectedly, abolishing HDAC3 catalytic activity by missense mutations in the nuclear receptor corepressor (NCOR or SMRT) does not cause infertility, despite causing histone hyperacetylation as HDAC3 knockout, demonstrating that HDAC3 enzyme activity is not required for spermatogenesis. Motif analysis of the HDAC3 cistrome in the testes identified SOX30, which has a similar spatiotemporal expression pattern as HDAC3 during spermatogenesis. Depletion of SOX30 in the testes abolishes the genomic recruitment of the HDAC3 to the binding sites. Collectively, these results establish the SOX30/HDAC3 signaling as a key regulator of the transcriptional program in a deacetylase-independent manner during the meiotic-to-postmeiotic transition in spermatogenesis.
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