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The finding that levels of Sry were lower in sex-reversed B6.Ytir gonads than in non-sex-reversed B6-Ydom strains suggests that low levels and/or mistiming of Sry may cause failure of testis differentiation. However, Lee and Taketo observed that levels of Sry in normal male gonads of the C57BL/6J strain are as low as in the B6-Ytir gonad, suggesting that low levels of Sry transcripts cannot be the sole cause of B6-Ytir sex reversal. Thus the molecular events underlying sex reversal in the B6-Ytir mouse still remain to be elucidated. SOX9, a SRT-related gene, was originally identified as responsible for campomelic dysplasia, a severe form of dwarfism often associated with XY male-to-female sex reversal. Like SRY, dosage may be important for proper function of SOX9, since mutations in humans appear to be present in only one allele, suggesting that sex reversal and campomelic dysplasia could be due to haploinsuffi-ciency of this gene product. Sox9 has been detected in the mouse urogenital complex of both sexes at 10.5 dpc. Beginning at 11.5 dpc, just after Sry is expressed in the male gonad, Sox9 is up-regulated in male gonads and down-regulated in female gonads.