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Rnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice

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 sperma...

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Detalles Bibliográficos
Autores principales: Xu, Longchang, Lu, Yalan, Han, Deqiang, Yao, Rongyan, Wang, Han, Zhong, Shunshun, Luo, Yanyun, Han, Ruiqin, Li, Kai, Fu, Jun, Zong, Shudong, Miao, Shiying, Song, Wei, Wang, Linfang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520686/
https://www.ncbi.nlm.nih.gov/pubmed/28518149
http://dx.doi.org/10.1038/cddis.2017.110
Descripción
Sumario: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.