Authors
Rui-Jie Ma, Meng-Meng Tang, Ping-Shuang Lu, Hao-Lin Zhang, Jia-Qian Ju, Ya-Ping Wang, Kun-Huan Zhang, Yue Wang, Shao-Chen Sun
Published in
Journal of cell science. Aug 10, 2026. Epub Aug 10, 2026.
Abstract
TRIM28, a member of the tripartite motif (TRIM) family, functions as a transcriptional coregulator involved in maintaining genome stability during mitosis. However, transcriptional activity is barely detectable during oocyte meiotic maturation. In this study, we explored the role of TRIM28 in mouse oocytes and found that it was constitutively expressed in the early stages of oocyte meiotic maturation, with predominant nuclear localization in germinal vesicle (GV)-stage oocytes. TRIM28 depletion caused defective germinal vesicle breakdown (GVBD), but oocytes that successfully underwent GVBD displayed unimpaired first polar body (PB1) extrusion. TRIM28 depletion impaired CDK1 activity and reduced cyclin B1 levels, leading to a delay in the G2/M transition. This delay may be attributed to altered levels of HDAC2-mediated H4K12ac and H3K4me2-modulated H3K9me2 in nonsurrounded nucleolus (NSN)-type GV oocytes, which decreased transcription activity. Additionally, TRIM28-depleted oocytes exhibited elevated γ-H2A.X expression, accompanied by aberrant expression of CHK1 and CHK2, as well as dysregulated expression of RAD51, which were collectively contributed to GVBD failure in mouse oocytes. In conclusion, our findings indicate that TRIM28 participates in the regulation of the G2/M transition during mouse oocyte meiotic maturation, acting through the modulation of histone modifications and DNA damage repair.
PMID:
42572494
Bibliographic data and abstract were imported from PubMed on 10 Aug 2026.
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