biostudies-literatureUnknown8(5)Xu LSpermatogenesis, 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 testiCell death & diseasee2795https://www.ebi.ac.uk/biostudies/studies/S-EPMC5520686biostudies-literatureRnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice.PMC5520686Xu LZong SHan RLu YMiao SYao RWang HLi KWang LZhong SFu JLuo YHan DSong WfalseRnf138 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 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 testi2017-01-01T00:00:00Z2017 May2026-05-06T01:18:01.295Z2019-03-27T00:09:04ZS-EPMC55206862851814910.1038/cddis.2017.110