BAX-DEFICIENT MICE WITH LYMPHOID HYPERPLASIA AND MALE GERM-CELL DEATH

BAX, a heterodimeric partner of BCL2, counters BCL2 and promotes apopt osis in gain-of-function experiments, A Bax knockout mouse was generat ed that proved viable but displayed lineage-specific aberrations in ce ll death, Thymocytes and B cells in this mouse displayed hyperplasia, and Bax-deficient ovaries contained unusual atretic follicles with exc ess granulosa cells. In contrast, Bax-deficient males were infertile a s a result of disordered seminiferous tubules with an accumulation of atypical premeiotic germ cells, but no mature haploid sperm, Multinucl eated giant cells and dysplastic cells accompanied massive cell death. Thus, the loss of Bax results in hyperplasia or hypoplasia, depending on the cellular context.