bcl-x is a member of the bcl-2 gene family, which may regulate program
med cell death. Mice were generated that lacked Bcl-x. The Bcl-x-defic
ient mice died around embryonic day 13. Extensive apoptotic cell death
was evident in postmitotic immature neurons of the developing brain,
spinal cord, and dorsal root ganglia. Hematopoietic cells in the liver
were also apoptotic. Analyses of bcl-x double-knockout chimeric mice
showed that the maturation of Bcl-x-deficient lymphocytes was diminish
ed. The life-span of immature lymphocytes, but not mature lymphocytes,
was shortened. Thus, Bcl-x functions to support the viability of imma
ture cells during the development oi the nervous and hematopoietic sys
tems.