Chinmo prevents male-to-female sex transformation of somatic stem cells in the adult Drosophila testis. Qing Ma¹, Matthew Wawersik², Erika Matunis¹. 1) Cell Biology Dept, The Johns Hopkins Sch Med, Baltimore, MD; 2) Biology Dept, The Col of William & Mary, Williamsburg, VA.

   Drosophila sexual identity is controlled cell-autonomously via activation of the Sex-lethal sex determination cascade in embryos and by non-autonomous signals that regulate sexual dimorphism throughout development. Once gender of an organ has been assigned, it is widely viewed as permanent. Here, we show that a downstream target of the Jak-STAT pathway, chronologically inappropriate morphogenesis (chinmo), is required for the active maintenance of male somatic cell identity in the adult testis. Partial reduction of Chinmo in the cyst stem cell (CySC) lineage of adult flies leads to a novel testis phenotype where germ cells over-proliferate and arrest as spermatogonia, and somatic cells form a layer of columnar epithelium that closely resembles the ovarian follicular epithelium. Lineage tracing shows that the columnar epithelium originates from squamous CySCs and cyst cells. This suggests that somatic cells acquire female identity in chinmo mutants while germ cells maintain male fate. Supporting this hypothesis, male form of Doublesex (DsxM), a male-specific somatic marker, is reduced in chinmo mutant CySCs and cyst cells. Additionally, the columnar epithelium in these mutants expresses ovarian follicle cell markers, while arrested germ cells express male specific markers, and RNAi of chinmo in the germline does not alter germ cell behavior. Also, loss of transformer, which is required for assignment of female fate in soma but not germline partially rescues the follicular epithelium phenotype in chinmo mutant testes. Thus, Chinmo plays a critical role in the maintenance of male fate in the adult Drosophila testis through the somatic sex determination pathway. Interestingly, the mammalian Dsx homolog Doublesex and mab-3 related transcription factor 1 (DMRT1) is required to maintain male identity in the testis of adult mice, but the mechanisms are not understood. Thus, our work may elucidate mechanisms that regulate sexual maintenance in other model systems.