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 , tw1 , tw5 , tw73), each causing embryonic death at a particular stage. Intercomplementation heterozygotes (txty) show ‘partial’ complementation, so that only some tyty offspring survive3,4. These survivors appear morphologically normal; indeed the females, being fertile, seem entirely normal. The txty males, however, are sterile. Among the reasons given for this sterility in some txty males are low motility of the txty spermatozoa5, and an inability to effect fertilization either in vitro or in vivo even when already present at the site of fertilization6,7. Spermatozoa from sterile txty 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 males5–8. 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 t6tw5 , t6tw32 and tw5tw32 (all ‘strong’ mutations2) and control mice clearly shows an even greater oligozoospermia (about 100 times less than controls) occurring in the txty males.