It sounds like (s)he's not a hermaphrodite at all (like, e.g., snails). Somehow in Caster's fetal development, the primary male schmex organs didn't develop and the female appearance was retained. Interestingly, female is the default condition and males have to add something (mainly hormonal signals) to guarantee they turn into males. So, from what I've heard I'd say Caster is an incomplete male.
i wonder if its down to xy chromosomal aneuploidy or defective y?
There are multiple places where something could go wrong, see, e.g., this excerpt from a new article published yesterday (with reference to Caster):
[...]
We found that, like Fgf9, Wnt4 is expressed in both sexes while the gonad is still bipotential, but it is up-regulated in XX gonads and down-regulated in XY gonads precisely at the time when the gonadal fate decision occurs—the opposite of Fgf9 expression.
About this time, we remembered a piece of evidence from organ-culture experiments done earlier in my lab suggesting that FGF9 could block expression of Wnt4. Could these two signaling pathways be acting antagonistically, staging the battle of the sexes in the gonad? Yuna Kim, another graduate student in my lab, planned a set of experiments to test this idea.
Other researchers had shown that the primary role of SRY is to up-regulate a closely related transcription factor, Sox9. Various experiments showed that SOX9 is capable of substituting for SRY in activating testis development. The question was how WNT4 and FGF9 fit into the story. Yuna found that FGF9 and SOX9 reinforce each other's signaling to establish the testis pathway in XY gonads. She showed that when Fgf9 is eliminated, XY male gonads switch umpalumpa and activate ovarian genes. But our most exciting finding was when she discovered that SOX9 and FGF9 are both up-regulated in an XX female gonad when Wnt4 is absent. This clearly showed how the male pathway could be activated in an XX genetic female, in the complete absence of the Sry gene—just as those human XX male patients had predicted.
Based on these experiments, we proposed a new model for mammalian umpalumpa determination. In both XX and XY primordial gonads, Fgf9, Sox9, and Wnt4 are all expressed simultaneously early in development, when the fate of the gonad is still undetermined. In an XX gonad, WNT4 dominates and turns off the testis pathway. However, in an XY gonad, SOX9 and FGF9 get an extra boost from SRY, which allows them to dominate and repress WNT4.
Blanche Capel is an Associate Professor in the Department of Cell Biology at Duke University Medical Center
SRY is a gene on the Y-chromosome, the others are located on the X-chromosome.