ArticleBiological research2024
The crucial role of HFM1 in regulating FUS ubiquitination and localization for oocyte meiosis prophase I progression in mice.
Article in Biological research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Transcriptomic signatures reveal systemic adaptations and immune modulation in response to training and competitive racing in horses.Equine veterinary journal · 2026Article
- Emerging role of FUS in TGFB1 and COL1A1 transcription dependent on GADD45B to induce NASH-fibrosis.Journal of molecular cell biology · 2026Article
- A homozygous variant in HFM1 causes preimplantation embryo developmental arrest by disrupting zygotic genome activation.Human reproduction (Oxford, England) · 2026Article
- Dosage effect of copy number variation in epilepsy and ten regions of the human brain.Scientific reports · 2025Article
- Novel biallelic HFM1 variants cause severe oligozoospermia with favorable intracytoplasmic sperm injection outcome.Asian journal of andrology · 2025Article
- HFM1 is essential for the germ cell intercellular bridge transport in primordial follicle formation in mice.Cellular and molecular life sciences : CMLS · 2024Article
- Granulosa cells provide transcriptomic information on ovarian follicle dynamics in southern white rhinoceros.Scientific reports · 2024Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundHelicase for meiosis 1 (HFM1), a putative DNA helicase expressed in germ-line cells, has been reported to be closely associated with premature ovarian insufficiency (POI). However, the underlying molecular mechanism has not been clearly elucidated. The aim of this study was to investigate the function of HFM1 in the first meiotic prophase of mouse oocytes.
resultsThe results suggested that the deficiency of HFM1 resulting in increased apoptosis and depletion of oocytes in mice, while the oocytes were arrested in the pachytene stage of the first meiotic prophase. In addition, impaired DNA double-strand break repair and disrupted synapsis were observed in the absence of HFM1. Further investigation revealed that knockout of HFM1 promoted ubiquitination and degradation of FUS protein mediated by FBXW11. Additionally, the depletion of HFM1 altered the intranuclear localization of FUS and regulated meiotic- and oocyte development-related genes in oocytes by modulating the expression of BRCA1.
conclusionsThese findings elaborated that the critical role of HFM1 in orchestrating the regulation of DNA double-strand break repair and synapsis to ensure meiosis procession and primordial follicle formation. This study provided insights into the pathogenesis of POI and highlighted the importance of HFM1 in maintaining proper meiotic function in mouse oocytes.
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