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Publication : Rnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice.

First Author  Xu L Year  2017
Journal  Cell Death Dis Volume  8
Issue  5 Pages  e2795
PubMed ID  28518149 Mgi Jnum  J:315603
Mgi Id  MGI:6829357 Doi  10.1038/cddis.2017.110
Citation  Xu L, et al. (2017) Rnf138 deficiency promotes apoptosis of spermatogonia in juvenile male mice. Cell Death Dis 8(5):e2795
abstractText  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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