RNF20 is required for male fertility through regulation of H2B ubiquitination in the Sertoli cells

BackgroundSpermatogenesis depends on the supporting of the Sertoli cells and their communications with germ cells. However, the regulation of crosstalk between the Sertoli cells and germ cells remains unclear.ResultsIn this report, we used conditional knockout technology to generate the Sertoli cells-specific knockout of Rnf20 in mice. The Amh-Rnf20(-/-) male mice were infertile owing to spermatogenic failure that mimic the Sertoli cell-only syndrome (SCOS) in humans. Knockout of Rnf20 resulted in the H2BK120ub loss in the Sertoli cells and impaired the transcription elongation of the Cldn11, a gene encoding a component of tight junction. Notably, RNF20 deficiency disrupted the cell adhesion, caused disorganization of the seminiferous tubules, and led to the apoptotic cell death of both spermatogonia and spermatocytes in the seminiferous tubules.ConclusionsThis study describes a Rnf20 knockout mouse model that recapitulates the Sertoli cell-only syndrome in humans and demonstrates that RNF20 is required for male fertility through regulation of H2B ubiquitination in the Sertoli cells.

Automated summary

In this study, a mouse model with Sertoli cells-specific knockout of Rnf20 was generated using conditional knockout technology. The Amh-Rnf20(-/-) male mice exhibited infertility due to spermatogenic failure, resembling the Sertoli cell-only syndrome in humans. Knockout of Rnf20 resulted in loss of H2BK120ub in the Sertoli cells, impairing the transcription elongation of Cldn11, a gene encoding a component of tight junction. Importantly, RNF20 deficiency disrupted cell adhesion, caused disorganization of seminiferous tubules, and induced apoptotic cell death in spermatogonia and spermatocytes.