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Sprouty2 Is Involved in Male Sex Organogenesis by Controlling Fibroblast Growth Factor 9-Induced Mesonephric Cell Migration to the Developing Testis

Department of Biochemistry (L.C., P.I., S.Z., S.V.), University of Oulu, FIN-90014 Oulu, Finland; and Department of Medical Biochemistry and Molecular Biology (L.C., P.I., S.V.), Biocenter Oulu, Laboratory of Developmental Biology, University of Oulu, FIN-90014, Oulu, Finland

Address all correspondence and requests for reprints to: Prof. Seppo Vainio, Biocenter Oulu, Laboratory of Developmental Biology, P.O. Box 5000, Aapistie 5A, FIN-90014 University of Oulu, Finland. E-mail: seppo.vainio{at}oulu.fi.

Fibroblast growth factor 9 (FGF9) signal has a role in organogenesis of the mammalian testis by controlling migration of mesonephric cells to the XY gonad, but neither it nor the FGF receptors is expressed sex-specifically. Of the Sprouty genes encoding antagonists of receptor tyrosine kinases including FGFr, mSprouty2 expression was confined to the developing testis and mesonephros. Gain of SPROUTY2 function in the male genital ridge and mesonephros malformed the vas deferens and epididymis, and diminished the number of seminiferous tubules and interstitium associating with reduced mesonephric cell migration and Fgf9 expression in embryonic testis, whereas exogenous FGF9 signaling recovered mesonephric cell migration inhibited by SPROUTY2. These phenotypes associated also with the decreased expression of Sox9, Desert hedgehog, Hsd3ß, Platelet/endothelial cell adhesion molecule, and -smooth muscle actin, which are markers of the Sertoli, Leydig, endothelial, and peritubular myoid cells of the developing testis. Based on these data, we propose that the Sprouty proteins are involved normally in mediating the sexually dimorphic signaling of FGF9 and controlling cell migration from the mesonephros during testis development.

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