Rnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice

Rnf138 缺陷促进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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