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is the most precise known parameter in sex determination. Indeed, analysis of the full Y chromosome has shown that there is variation in the number of repeats and other features, which complicate precise analysis. As an example, the SRY sequence is found in only half the copies. Analysis of the unique sequence of the gene OCT1 has further proven problematic. As another example, the XIST gene is not located on the sex chromosomes, but instead on the X chromosome. This gene is expressed in females, and has been implicated in the inactivation of the X chromosome in females, yet its role in males has not been clearly defined. Additionally, genes found on the Y chromosome have not been shown to have a role in human sexual development. (Li, Yang et al. (2001) Nature 412:710-716). The Sry gene located on the Y chromosome is responsible for development of the testes in males. Many, but not all, sex-linked traits in humans are not due to mutations in the SRY gene. Because SRY is a testis-determining factor in the male, the majority of mutations affecting sex determination in humans occur outside the SRY gene and the testis-determining pathway. Given that SRY is a direct determinant of spermatogenesis in males, a number of characteristics of the SRY gene and the Y chromosome suggest that mutations in SRY might cause defects in sperm maturation. Initial evidence for defects in sperm came from the analysis of sex-linked aneuploidy, which is more common in sons of fathers with mutations in the SRY gene. Polymorphisms in the SRY gene have been observed in all human populations studied, indicating a strong evolutionary pressure. In addition, mutations in the SRY gene are a major cause of male infertility and affect 10% of infertile men. These observations have led to the suggestion that SRY function in spermatogenesis may have led to a constraint on its evolution and a requirement for very tight regulation. (Zhu, Luu et al. (1997) Hum. Mol. Genet. 6:1773-1776). In a similar manner, mutations in the FOXL2 gene on the X chromosome have been shown to lead to malformations of the ovaries, including premature ovarian failure. (WO 99/24455). Additionally, mutations in the WNT4 gene on the X chromosome are associated with sex reversal in humans and mice, and mutations in
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