Boys, girls and shuttling of SRY and SOX9

  • Sim H
  • Argentaro A
  • Harley V
  • 68

    Readers

    Mendeley users who have this article in their library.
  • 46

    Citations

    Citations of this article.

Abstract

In the mammalian embryo, SRY and SOX9 are key Sertoli cell proteins that drive the development of the bipotential gonad into a testes rather than an ovary, leading ultimately to the male phenotype. Clinical SRY and SOX9 mutations causing disorders of sex development (DSD) highlight defective protein-protein interactions between SRY or SOX9, and carrier proteins required for nuclear import (importin-b and calmodulin) and nuclear export (CRM-1). The fine balance between import and export determines the levels of transcriptionally active SRY and SOX9 in the nucleus. Recently, post-translational modifications of SRY and SOX9 have been identified which affect nuclear transport. It is therefore timely that the consequences of sex-reversal mutation upon nuclear transport be reviewed. SRY and SOX9 mutations in DSD have uncovered regulatory sites for sumoylation, ubiquitination, acetylation and phosphorylation, many of which are essential for their transport and sex determining functions. © 2008 Elsevier Ltd. All rights reserved.

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

Authors

  • Helena Sim

  • Anthony Argentaro

  • Vincent R. Harley

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free