Evidence from Tfm/0 that Androgen is Inessential for Reproduction in Female Mice

Abstract

THE testicular feminisation syndrome in affected XY male mice is the result of the action of the X-linked Tfm gene¹, which causes a failure of target organs to respond to androgen. The question arises whether genetic females affected with the gene would be reproductively abnormal in any way. Androgen is produced in the normal mouse ovary; its functional significance is not understood but it has been claimed that a response to androgen is essential for ovulation and mating². If so, then females homozygous or hemizygous for the Tfm gene (Tfm/Tfm or Tfm/0) might be unable to reproduce. Ohno et al.³, have recently described six Tfm/0 female mice which collectively showed remarkably rapid ovarian degeneration, more rapid than in +/0 mice, thus leading to the conclusion that a response to androgen is necessary for normal ovarian function in mice. The fertility of these mice had not, however, been tested. We here report results with two Tfm/0 mice, both of which proved to be fertile and produced litters.