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Rnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice.

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
Cell death & disease | 2017

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.

Pubmed ID: 28518149

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