Testis determination requires insulin receptor family function in mice

Serge Nef, Sunita Verma-Kurvari, Jussi Merenmies, Jean-Dominique Vassalli, Argiris Efstratiadis, Domenico Accili and Luis F. Parada ()
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Serge Nef: University of Texas, Southwestern Medical Center
Sunita Verma-Kurvari: University of Texas, Southwestern Medical Center
Jussi Merenmies: University of Texas, Southwestern Medical Center
Jean-Dominique Vassalli: University of Geneva
Argiris Efstratiadis: College of Physicians & Surgeons of Columbia University
Domenico Accili: College of Physicians & Surgeons of Columbia University
Luis F. Parada: University of Texas, Southwestern Medical Center

Nature, 2003, vol. 426, issue 6964, 291-295

Abstract: Abstract In mice, gonads are formed shortly before embryonic day 10.5 by the thickening of the mesonephros and consist of somatic cells and migratory primordial germ cells1. The male sex-determining process is set in motion by the sex-determining region of the Y chromosome (Sry), which triggers differentiation of the Sertoli cell lineage. In turn, Sertoli cells function as organizing centres and direct differentiation of the testis. In the absence of Sry expression, neither XX nor XY gonads develop testes2, and alterations in Sry expression are often associated with abnormal sexual differentiation3,4,5,6,7,8. The molecular signalling mechanisms by which Sry specifies the male pathway and models the undifferentiated gonad are unknown. Here we show that the insulin receptor tyrosine kinase family, comprising Ir, Igf1r and Irr, is required for the appearance of male gonads and thus for male sexual differentiation. XY mice that are mutant for all three receptors develop ovaries and show a completely female phenotype. Reduced expression of both Sry and the early testis-specific marker Sox9 indicates that the insulin signalling pathway is required for male sex determination.

Date: 2003
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DOI: 10.1038/nature02059

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