The BCL-2 family has Various pairs of antagonist and agonist proteins
that regulate apoptosis, Whether their function is interdependent is u
ncertain. Using a genetic approach to address this question, we utiliz
ed gain- and loss-of-function models of Bcl-2 and Bar and found that a
poptosis and thymic hypoplasia characteristic of Bcl-2-deficient mice
are largely absent in mice also deficient in Bax. A single copy of Bar
promoted apoptosis in the absence of Bcl-2. In contrast, overexpressi
on of Bcl-2 still repressed apoptosis in the absence of Bax. While an
in vivo competition exists between Bar and Bcl-2, each is able to regu
late apoptosis independently.