Rnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice

Rnf138 缺乏导致幼年雄性小鼠精原细胞凋亡

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作者:Longchang Xu, Yalan Lu, Deqiang Han, Rongyan Yao, Han Wang, Shunshun Zhong, Yanyun Luo, Ruiqin Han, Kai Li, Jun Fu, Shudong Zong, Shiying Miao, Wei Song, Linfang Wang

Abstract

Spermatogenesis, the process by which haploid sperm cells are produced from a diploid precursor cell, is essential for sexual reproduction. Here, we report that RING-finger protein 138 (Rnf138) is highly expressed in testes, especially in spermatogonia and spermatocytes. The role of Rnf138 in spermatogenesis was examined using a Rnf138-knockout mouse model. Rnf138 deficiency resulted in increased apoptosis in spermatogenic cells, loss of proliferative spermatogonia, delayed development of spermatozoa and impaired fertility. The proportion of PLZF+Ki67+ cells within the PLZF+ population decreased in the knockout mice. The phenotype was further assessed by RNA-sequencing (RNA-seq), which determined that the expression levels of many genes involved in spermatogenesis were altered in the testis of Rnf138-knockout mice. Thus, Rnf138 deficiency promotes the apoptosis of spermatogenic cells, which may have been caused by the aberrant proliferation of spermatogonia in mouse testis development.

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