Explanation of sterility in t^xt^y male mice

Abstract

The lethal ‘t alleles’ of the T complex on mouse chromosome 17 (refs 1, 2) have been assigned to six complementation groups (the definitive classes being t⁰ , t⁹ , t¹² , t^w1 , t^w5 , t^w73), each causing embryonic death at a particular stage. Intercomplementation heterozygotes (t^xt^y) show ‘partial’ complementation, so that only some t^yt^y offspring survive^3,4. These survivors appear morphologically normal; indeed the females, being fertile, seem entirely normal. The t^xt^y males, however, are sterile. Among the reasons given for this sterility in some t^xt^y males are low motility of the t^xt^y spermatozoa⁵, and an inability to effect fertilization either in vitro or in vivo even when already present at the site of fertilization^6,7. Spermatozoa from sterile t^xt^y males were reported to be apparently present in ‘normal’ numbers in the uterus, although actual ejaculate numbers have not been quoted for these, or indeed for normal fertile males^5–8. In the human, typical ejaculate counts of less than 20 × 10⁶ spermatozoa, where the normal ejaculate contains 100–250 × 10⁶, are judged to indicate clinical sterility⁹. The comparison of numbers of spermatozoa¹⁰ ejaculated into the female tract by sterile t⁶t^w5 , t⁶t^w32 and t^w5t^w32 (all ‘strong’ mutations²) and control mice clearly shows an even greater oligozoospermia (about 100 times less than controls) occurring in the t^xt^y males.