International Mammalian Genome Society

The 16th International Mouse Genome Conference (2002)

Oral Presentation

Tuesday 19 November

11:30 - 11:45 HRS


Y Qin
Baylor College of Medicine

Co-Authors: Troung C, Bishop CE
Institutions: Baylor College of Medicine

Loss of Fgf9 has been shown to cause XY sex reversal, acting downstream of Sry to stimulate mesenchymal proliferation, mesonephric cell migration and Sertoli cell differentiation in fetal testis. Sox9 also plays a critical role in sex determination causing XX sex reversal when expressed in XX transgenic mice, or in XX Ods/+ (Odd Sex) mutant mice which constitutively express Sox9 in fetal gonads. In order to examine the relationship between these two genes in the sex determination pathway, we examined the expression of Fgf9 in XX Ods/+ male gonads between E12.5E14.5. Surprisingly, it was found to be undetectable, whereas Sox9 was normally expressed. We also bred female Fgf9+/- mice to XY Ods+/- carrier males to produce XY Fgf9-/-, XY Ods/+ Fgf9-/-, and XX Ods/+ Fgf9-/- mice. As reported, XY Fgf9-/- mice showed a female phenotype whereas XX or XY Ods/+, Fgf9-/- mice appeared fully masculinized i.e. Sox9 could rescue the XY Fgf9-/- sex reversal but Fgf9 loss could not reverse the sex of XX Ods/+ males. This suggests that Fgf9 must act between Sry and Sox9 in the sex determining pathway, and that the full phenotypic rescue of Fgf9 loss has occurred due to expression of Sox9. These data indicate that Fgf9 expression may not be important to sex determination per se, but rather acts by upregulating the levels of Sox9 expression. In XX Ods mice, which express Sox9 via another mechanism, Fgf9 loss does not seem important to sex determination.

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