In addition, we are studying autosomal defects that cause severe spermatogenic failure in mice. The proteins likely function as sequence-specific activators of transcription. ZFY and ZFX were originally implicated in sex determination, but present evidence argues against such a role. Instead, our gene targeting experiments in mice suggest that ZFX contributes to early embryonic growth, animal size, and germ cell number in both males and females. In females, one X chromosome is silenced by X inactivation, a process often assumed to have evolved on a broadly regional or chromosomal basis.
Many extant genes appear to be intermediates.
Further, we suspect that, for each gene or cluster, X inactivation was an adaptation to decay of an homologous, Y-linked gene. Diverse spermatogenic defects in humans caused by overlapping, de novo Y deletions that encompass a novel RNA-binding protein gene. Saxena, R., et al. The DAZ gene cluster on the human Y chromosome arose from an autosomal gene that was transposed, then repeatedly amplified and pruned. D.C. Zfx mutation results in small animal size and reduced germ cell number in male and female mice.