ArticleHuman molecular genetics2015
FANCB is essential in the male germline and regulates H3K9 methylation on the sex chromosomes during meiosis.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 78 citations in OpenAlex.
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- Gene set enrichment analysis of curated monogenic loci highlights key pathways and multisystem involvement in male infertility.Basic and clinical andrology · 2026Article
- MCM8-9 helicase activity protects primordial germ cell development to prevent premature ovarian insufficiency.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Massive Genomic and Transcriptomic Changes Within a Young Inversion Polymorphism in the Absence of Degeneration.Molecular ecology · 2026Article
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- Searching for the 'X' factor: investigating the genetics of primary ovarian insufficiency.Journal of ovarian research · 2024Review
- Single-cell transcriptomic and cross-species comparison analyses reveal distinct molecular changes of porcine testes during puberty.Communications biology · 2024Article
- Whole exome sequencing analysis of 167 men with primary infertility.BMC medical genomics · 2024Article
- Fance deficiency impaired DNA damage repair of prospermatogonia and altered the repair dynamics of spermatocytes.Reproductive biology and endocrinology : RB&E · 2024Article
- PRC1 directs PRC2-H3K27me3 deposition to shield adult spermatogonial stem cells from differentiation.Nucleic acids research · 2024Article
- Novel compound heterozygous variants in FANCI cause premature ovarian insufficiency.Human genetics · 2024Article
- The DNA helicase FANCJ (BRIP1) functions in double strand break repair processing, but not crossover formation during prophase I of meiosis in male mice.PLoS genetics · 2024Article
- Research progress on the fanconi anemia signaling pathway in non-obstructive azoospermia.Frontiers in endocrinology · 2024Review
- A comprehensive analysis of Fanconi anemia genes in Chinese patients with high-risk hereditary breast cancer.Journal of cancer research and clinical oncology · 2023Article
- The DNA helicase FANCJ (BRIP1) functions in Double Strand Break repair processing, but not crossover formation during Prophase I of meiosis in male mice.bioRxiv : the preprint server for biology · 2023Article
- FAAP100 is required for the resolution of transcription-replication conflicts in primordial germ cells.BMC biology · 2023Article
- Article
- Sertoli cell-only syndrome: advances, challenges, and perspectives in genetics and mechanisms.Cellular and molecular life sciences : CMLS · 2023Review
- Sex body: A nest of protein mixture.Frontiers in cell and developmental biology · 2023Review
- Whole-genome sequencing identifies new candidate genes for nonobstructive azoospermia.Andrology · 2022Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Fanconi anemia (FA) is a recessive X-linked and autosomal genetic disease associated with bone marrow failure and increased cancer, as well as severe germline defects such as hypogonadism and germ cell depletion. Although deficiencies in FA factors are commonly associated with germ cell defects, it remains unknown whether the FA pathway is involved in unique epigenetic events in germ cells. In this study, we generated Fancb mutant mice, the first mouse model of X-linked FA, and identified a novel function of the FA pathway in epigenetic regulation during mammalian gametogenesis. Fancb mutant mice were infertile and exhibited primordial germ cell (PGC) defects during embryogenesis. Further, Fancb mutation resulted in the reduction of undifferentiated spermatogonia in spermatogenesis, suggesting that FANCB regulates the maintenance of undifferentiated spermatogonia. Additionally, based on functional studies, we dissected the pathway in which FANCB functions during meiosis. The localization of FANCB on sex chromosomes is dependent on MDC1, a binding partner of H2AX phosphorylated at serine 139 (γH2AX), which initiates chromosome-wide silencing. Also, FANCB is required for FANCD2 localization during meiosis, suggesting that the role of FANCB in the activation of the FA pathway is common to both meiosis and somatic DNA damage responses. H3K9me2, a silent epigenetic mark, was decreased on sex chromosomes, whereas H3K9me3 was increased on sex chromosomes in Fancb mutant spermatocytes. Taken together, these results indicate that FANCB functions at critical stages of germ cell development and reveal a novel function of the FA pathway in the regulation of H3K9 methylation in the germline.
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