Bid is a BH3 domain only pro-apoptotic member of the Bcl-2 family which int
eracts with Ba-x to regulate apoptosis. Bax-deficient embryos show decrease
d neuronal programmed cell death in vivo and resistance to cytosine arabino
side (AraC)-induced neuronal apoptosis in vitro. In this report, we demonst
rate that Bid-deficient embryos show no neurodevelopmental abnormalities, a
nd Bid-deficiency has no effect on the in vitro apoptotic response of eithe
r telencephalic neural precursor cells or neurons to AraC-induced death. We
conclude that bid does not play an essential role in either naturally occu
rring or genotoxin-induced neuronal cell death. (C) 2001 Elsevier Science B
Y All rights reserved.