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¹ Division of Sex Differentiation, National Institute for Basic Biology, Okazaki 444-8787, Japan
² School of Life Science, The Graduate University for Advanced Studies, Okazaki 444-8585, Japan
³ Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Kawaguchi 332-0012, Japan
⁴ Laboratory of Molecular and Cellular Biology, Department of Life Science, Faculty of Bioresources, Mie University, Tsu 514-8507, Japan
⁵ Technology and Development Team for Mammalian Cellular Dynamics, BioResource Center, RIKEN Tsukuba Institute, Tsukuba 305-0074, Japan
⁶ Laboratory of Animal Physiology, Graduate School of Bioagricultural Sciences, Nagoya University, Chikusa, Nagoya 464-8601, Japan

Recent loss-of-function and gain-of-function studies have revealed that transcription factor Sox9 is required for testis formation by governing Sertoli cell differentiation, and thereafter regulating transcription of Sertoli marker genes. In the present study, we identified a novel isoform of Vinexin, which is expressed in somatic cells but not germ cells of sexually indifferent stages of fetal gonads. After the sex is determined, the expression continues in testicular Sertoli cells. Immunohistochemical analyses with a specific antibody to Vinexin indicated that Vinexin is localized in the cytoplasm. Functional studies with C3H10T1/2 cells showed that Vinexin acted as a scaffold protein to activate MEK and ERK through interaction with c-Raf and ERK. Ultimately, Sox9 transcription was induced by Vinexin . This up-regulation of Sox9 expression disappeared when the cells were treated with a specific MEK inhibitor, U0126. To determine the role of Vinexin during gonad formation, the gene was disrupted by targeted mutagenesis. The phenotype displayed by the mice indicated that ERK activation was decreased in the Vinexin ^–/– XY gonads, and Sox9 expression was down-regulated. Thus, Vinexin seems to be implicated in regulation of Sox9 gene expression by modulating MAPK cascade in mouse fetal gonads.

^* Correspondence: E-mail: moro{at}nibb.ac.jp

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