ArticleCell death & disease2020
UHRF1-repressed 5'-hydroxymethylcytosine is essential for the male meiotic prophase I.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- The intricate dance of RNA-binding proteins: unveiling the mechanisms behind male infertility.Human reproduction update · 2026Review
- Analysis of DNA methylation changes following Cfp1 knockout in mouse spermatocytes.Animal bioscience · 2025Article
- E3 Ubiquitin LigaseInternational journal of molecular sciences · 2024Article
- Single-cell multi-omics sequencing of human spermatogenesis reveals a DNA demethylation event associated with male meiotic recombination.Nature cell biology · 2023Article
- UHRF1 is a mediator of KRAS driven oncogenesis in lung adenocarcinoma.Nature communications · 2023Article
- UHRF1 interacts with snRNAs and regulates alternative splicing in mouse spermatogonial stem cells.Stem cell reports · 2022Article
- UHRF1 establishes crosstalk between somatic and germ cells in male reproduction.Cell death & disease · 2022Article
- Proteolysis in Reproduction: Lessons From Gene-Modified Organism Studies.Frontiers in endocrinology · 2022Review
- Article
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19 authors at 4 institutions in 1 country.
Funding
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Abstract
5'-hydroxymethylcytosine (5hmC), an important 5'-cytosine modification, is altered highly in order in male meiotic prophase. However, the regulatory mechanism of this dynamic change and the function of 5hmC in meiosis remain largely unknown. Using a knockout mouse model, we showed that UHRF1 regulated male meiosis. UHRF1 deficiency led to failure of meiosis and male infertility. Mechanistically, the deficiency of UHRF1 altered significantly the meiotic gene profile of spermatocytes. Uhrf1 knockout induced an increase of the global 5hmC level. The enrichment of hyper-5hmC at transcriptional start sites (TSSs) was highly associated with gene downregulation. In addition, the elevated level of the TET1 enzyme might have contributed to the higher 5hmC level in the Uhrf1 knockout spermatocytes. Finally, we reported Uhrf1, a key gene in male meiosis, repressed hyper-5hmC by downregulating TET1. Furthermore, UHRF1 facilitated RNA polymerase II (RNA-pol2) loading to promote gene transcription. Thus our study demonstrated a potential regulatory mechanism of 5hmC dynamic change and its involvement in epigenetic regulation in male meiosis.
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