ArticleeLife2024
FBXO24 modulates mRNA alternative splicing and MIWI degradation and is required for normal sperm formation and male fertility.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 6 citations in OpenAlex.
- Testis-Enriched F-Box Protein FBXO39 Is Important for Spermiogenesis and Male Fertility in Mice.Andrology · 2026Article
- The deubiquitinase USP4 stabilizes the SCFNature communications · 2026Article
- Hsa-circ_0081481-miR 3960-FBXO24 regulatory axis in non-obstructive azoospermia identifies potential biomarkers of spermatogenic failure.Scientific reports · 2026Article
- FBXO39 knockdown promotes spermatogenesis impairment by inducing mitochondrial dysfunction and ferroptosis via inhibiting KDM5A ubiquitination and regulating H3K4me3 demethylation.Cell biology and toxicology · 2026Article
- Mutation Severity ofHuman mutation · 2026Article
- Reciprocal Regulation Between the SCFbioRxiv : the preprint server for biology · 2025Article
- Transposable Elements Drive Regulatory and Functional Innovation of F-box Genes.Molecular biology and evolution · 2025Article
- The Intricate Functional Networks of Pre-mRNA Alternative Splicing in Mammalian Spermatogenesis.International journal of molecular sciences · 2024Review
- Article
- The emerging and diverse roles of F-box proteins in spermatogenesis and male infertility.Cell regeneration (London, England) · 2024Review
- FBXO24 deletion causes abnormal accumulation of membraneless electron-dense granules in sperm flagella and male infertility.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Spermiogenesis is a critical, post-meiotic phase of male gametogenesis, in which the proper gene expression is essential for sperm maturation. However, the underFlying molecular mechanism that controls mRNA expression in the round spermatids remains elusive. Here, we identify that FBXO24, an orphan F-box protein, is highly expressed in the testis of humans and mice and interacts with the splicing factors (SRSF2, SRSF3, and SRSF9) to modulate the gene alternative splicing in the round spermatids. Genetic mutation of FBXO24 in mice causes many abnormal splicing events in round spermatids, thus affecting a large number of critical genes related to sperm formation that were dysregulated. Further molecular and phenotypical analyses revealed that FBXO24 deficiency results in aberrant histone retention, incomplete axonemes, oversized chromatoid body, and abnormal mitochondrial coiling along sperm flagella, ultimately leading to male sterility. In addition, we discovered that FBXO24 interacts with MIWI and SCF subunits and mediates the degradation of MIWI via K48-linked polyubiquitination. Furthermore, we show that FBXO24 depletion could lead to aberrant piRNA production in testes, which suggests FBXO24 is required for normal piRNA counts. Collectively, these data demonstrate that FBXO24 is essential for sperm formation by regulating mRNA alternative splicing and MIWI degradation during spermiogenesis.
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Registered trials
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