ArticleNucleic acids research2022
Dual role of histone variant H3.3B in spermatogenesis: positive regulation of piRNA transcription and implication in X-chromosome inactivation.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- The eutherian-specific histone H3.4 promotes germ cell development and reproductive fitness.Nature communications · 2026Article
- DAXX directs dual modes of H3.4-to-H3.3 histone replacement in the male germline.Genes & development · 2026Article
- DAXX governs the silencing of LINE1 during spermatogenesis in mice.Nucleic acids research · 2026Article
- Article
- PBAF/cBAF reorganization on H3.3 chromatin regulates BMAL1 activity in the absence of circadian negative feedback.Nature communications · 2025Article
- 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
- Cracking the code: how piRNA pathway shapes spermatogenesis and combats male infertility.Frontiers in cell and developmental biology · 2025Review
- ARID1A governs the silencing of sex-linked transcription during male meiosis in the mouse.eLife · 2024Article
- The functions and mechanisms of piRNAs in mediating mammalian spermatogenesis and their applications in reproductive medicine.Cellular and molecular life sciences : CMLS · 2024Review
- Casting histone variants during mammalian reproduction.Chromosoma · 2023Review
- Linker histone variant H1.2 is a brake on white adipose tissue browning.Nature communications · 2023Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The histone variant H3.3 is encoded by two distinct genes, H3f3a and H3f3b, exhibiting identical amino-acid sequence. H3.3 is required for spermatogenesis, but the molecular mechanism of its spermatogenic function remains obscure. Here, we have studied the role of each one of H3.3A and H3.3B proteins in spermatogenesis. We have generated transgenic conditional knock-out/knock-in (cKO/KI) epitope-tagged FLAG-FLAG-HA-H3.3B (H3.3BHA) and FLAG-FLAG-HA-H3.3A (H3.3AHA) mouse lines. We show that H3.3B, but not H3.3A, is required for spermatogenesis and male fertility. Analysis of the molecular mechanism unveils that the absence of H3.3B led to alterations in the meiotic/post-meiotic transition. Genome-wide RNA-seq reveals that the depletion of H3.3B in meiotic cells is associated with increased expression of the whole sex X and Y chromosomes as well as of both RLTR10B and RLTR10B2 retrotransposons. In contrast, the absence of H3.3B resulted in down-regulation of the expression of piRNA clusters. ChIP-seq experiments uncover that RLTR10B and RLTR10B2 retrotransposons, the whole sex chromosomes and the piRNA clusters are markedly enriched of H3.3. Taken together, our data dissect the molecular mechanism of H3.3B functions during spermatogenesis and demonstrate that H3.3B, depending on its chromatin localization, is involved in either up-regulation or down-regulation of expression of defined large chromatin regions.
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