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The agouti-yellow ( A   y  ) deletion is the only genetic modifier known to suppress testicular germ cell tumor (TGCT) susceptibility in mice or humans. The  A   y   mutation deletes  Raly  and  Eif2s2 , and induces the ectopic expression of  agouti , all of which are potential TGCT-modifying mutations. Here we report that the reduced TGCT incidence of heterozygous  A   y   males and the recessive embryonic lethality of  A   y   are caused by the deletion of  Eif2s2 , the beta subunit of translation initiation factor eIF2. We found that the incidence of affected males was reduced 2-fold in mice that were partially deficient for  Eif2s2  and that embryonic lethality occurred near the time of implantation in mice that were fully deficient for  Eif2s2 . In contrast, neither reduced expression of  Raly  in gene-trap mice nor ectopic expression of  agouti  in transgenic or viable-yellow ( A   vy  ) mutants affected TGCT incidence or embryonic viability. In addition, we provide evidence that partial deficiency of  Eif2s2  attenuated germ cell proliferation and differentiation, both of which are important to TGCT formation. These results show that germ cell development and TGCT pathogenesis are sensitive to the availability of the eIF2 translation initiation complex and to changes in the rate of translation.

Deletion of eIF2beta suppresses testicular cancer incidence and causes recessive lethality in agouti-yellow mice