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Submitted on March 7, 2006
Accepted on April 25, 2006
Department of Biochemistry, University of Oulu, P. O. Box 3000, FIN-90014 Oulu, Finland; Department of Medical Biochemistry and Molecular Biology, Biocenter Oulu, Laboratory of Developmental Biology, University of Oulu, P.O. Box 5000, FIN-90014, Oulu, Finland
* To whom correspondence should be addressed. E-mail: seppo.vainio{at}oulu.fi.
FGF9 signal has a role in organogenesis of the mammalian testis by controlling migration of mesonephric cells to the XY gonad but, neither it or the FGF receptors is expressed sex-specifically. Of the Sprouty genes encoding antagonists of receptor tyrosine kinases including FGFr, mSprouty2 expression confined to the developing testis and mesonephros. Gain of SPROUTY2 function in the male genital ridge and mesonephros malformed the vas deferens, epididymis, diminished the number of seminiferous tubules and interstitium associating with reduced mesonephric cell migration and FGF9 expression in embryonic testis, while exogenous FGF9 signaling recovered mesonephric cell migration inhibited by SPROUTY2. These phenotypes associated also with the decreased expression of Sox9, Desert hedgehog, Hsd3
, PECAM 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, controlling cell migration from the mesonephros during testis development.
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