| First Author | Shindler KS | Year | 1997 |
| Journal | J Neurosci | Volume | 17 |
| Issue | 9 | Pages | 3112-9 |
| PubMed ID | 9096145 | Mgi Jnum | J:39573 |
| Mgi Id | MGI:86927 | Doi | 10.1523/JNEUROSCI.17-09-03112.1997 |
| Citation | Shindler KS, et al. (1997) Bax deficiency prevents the increased cell death of immature neurons in bcl-x-deficient mice. J Neurosci 17(9):3112-9 |
| abstractText | The intracellular balance between pro- and antiapoptotic members of the Bcl-2 gene family is thought to regulate cell death. Targeted disruption of bcl-x, a death repressing member, causes massive cell death of immature neurons in the developing mouse CNS, whereas targeted disruption of bax, a pro-apoptotic member, blocks the death of specific populations of sympathetic and motor neurons. In the present study, mice deficient in both Bcl- x(L) and Bar (bcl-x(-/-)/bau(-/-)) are used to examine the relative significance and potential interactions of Bcl- x(L) and Bar during early CNS development. Bcl-x(-/-)/ bax(-/-) mice demonstrate greatly reduced levels of apoptosis both in vivo and in vitro compared with the CNS of Bcl-x(L)-deficient mice, as assessed by histology and terminal deoxytransferase-mediated deoxyuridine triphosphate nick end-labeling. Bax-deficient mice, however, contain occasional apoptotic cells in the developing CNS, and cultures of bax-deficient telencephalic cells demonstrate similar levels of apoptosis as wild-type cultures. These results suggest that Bar critically interacts with Bcl-x(L) to regulate survival of immature neurons, but indicate that other cell death regulating proteins, in addition to Bcl-x(L) and Bax, also function during CNS development. |
