Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 583, Issue -, Pages 169-177Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2021.10.074
Keywords
Spermatogonia; BMI1; PTPRM; Epigenetic mechanism
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Funding
- National Natural Science Foundation of China [81901532, 81901533]
- Natural Science Foundation of Jiangsu Province [BK20190188]
- Gusu Health Talent Program of Suzhou [GSWS2020068]
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BMI1 plays a crucial role in promoting spermatogonia proliferation and inhibiting apoptosis by binding to the promoter region of the PTPRM gene, driving chromatin remodeling and gene silencing, and improving spermatogonia maintenance. This provides potential therapeutic targets for the treatment of male infertility.
Spermatogonia are accountable for spermatogenesis and male fertility, but the underlying mechanisms involved in spermatogonia maintenance are not clear. B lymphoma Mo-MLV insertion region 1 (BMI1) is a key component of epigenetic silencers. BMI1 is essential for stem-cell maintenance. Here, we attempted to uncover the role of BMI1 in spermatogonia maintenance using a mouse spermatogonia cell line (GC-1) and Bmi1-knockout (KO) mouse model. We showed that BMI1 promoted the proliferation and inhibited apoptosis of GC-1 cells. Mechanistically, we present in vitro and in vivo evidence to show that BMI1 binds to the promoter region of the Protein tyrosine phosphatase receptor type M (PTPRM) gene, thereby driving chromatin remodeling and gene silencing. Knockdown of Ptprm expression significantly improved spermatogonia proliferation in BMI1-deficient GC-1 cells. Collectively, our data show, for the first time, an epigenetic mechanism involving in BMI1-mediated gene silencing in spermatogonia maintenance, and provide potential targets for the treatment of male infertility. (c) 2021 Elsevier Inc. All rights reserved.
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