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The new concept of mammalian sex maintenance establishes that particular key genes must remain active in the differentiated gonads to avoid genetic sex reprogramming, as described in adult ovaries after  Foxl2  ablation.  Dmrt1  plays a similar role in postnatal testes, but the mechanism of adult testis maintenance remains mostly unknown.  Sox9  and  Sox8  are required for postnatal male fertility, but their role in the adult testis has not been investigated. Here we show that after ablation of  Sox9  in Sertoli cells of adult, fertile  Sox8 -/-   mice, testis-to-ovary genetic reprogramming occurs and Sertoli cells transdifferentiate into granulosa-like cells. The process of testis regression culminates in complete degeneration of the seminiferous tubules, which become acellular, empty spaces among the extant Leydig cells. DMRT1 protein only remains in non-mutant cells, showing that SOX9/8 maintain  Dmrt1  expression in the adult testis. Also,  Sox9/8  warrant testis integrity by controlling the expression of structural proteins and protecting Sertoli cells from early apoptosis. Concluding, this study shows that, in addition to its crucial role in testis development , Sox9 , together with  Sox8  and coordinately with  Dmrt1 , also controls adult testis maintenance.

Sox9 and Sox8 protect the adult testis from male-to-female genetic reprogramming and complete degeneration