BAX Is Required for Neuronal Death after Trophic Factor Deprivation and during Development

Members of the BCL2-related family of proteins either promote or repress programmed cell death. BAX, a death-promoting member, heterodimerizes with multiple death-repressing molecules, suggesting that it could prove critical to cell death. We tested whether Bax is required for neuronal death by trop...

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Bibliographic Details
Published in:Neuron (Cambridge, Mass.) Mass.), 1996-09, Vol.17 (3), p.401-411
Main Authors: Deckwerth, Thomas L, Elliott, Jeffrey L, Knudson, C.Michael, Johnson, Eugene M, Snider, William D, Korsmeyer, Stanley J
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Axons - physiology
bcl-2-Associated X Protein
Cell Death - drug effects
Cell Death - genetics
Cell Lineage - physiology
Cell Survival - drug effects
Facial Nerve - cytology
Facial Nerve - surgery
Female
Gene Expression Regulation, Developmental - physiology
Hyperplasia - genetics
In Situ Hybridization
Lymphocytes - physiology
Male
Mice
Mice, Knockout
Motor Neurons - cytology
Motor Neurons - drug effects
Motor Neurons - physiology
Nerve Growth Factors - pharmacology
Ovary - pathology
Proto-Oncogene Proteins - genetics
Proto-Oncogene Proteins c-bcl-2
RNA, Messenger - metabolism
Sympathetic Nervous System - cytology
Testis - pathology
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Summary:Members of the BCL2-related family of proteins either promote or repress programmed cell death. BAX, a death-promoting member, heterodimerizes with multiple death-repressing molecules, suggesting that it could prove critical to cell death. We tested whether Bax is required for neuronal death by trophic factor deprivation and during development. Neonatal sympathetic neurons and facial motor neurons from Bax-deficient mice survived nerve growth factor deprivation and disconnection from their targets by axotomy, respectively. These salvaged neurons displayed remarkable soma atrophy and reduced elaboration of neurites; yet they responded to readdition of trophic factor with soma hypertrophy and enhanced neurite outgrowth. Bax-deficient superior cervical ganglia and facial nuclei possessed increased numbers of neurons. Our observations demonstrate that trophic factor deprivation–induced death of sympathetic and motor neurons depends on Bax.
ISSN:0896-6273
1097-4199
DOI:10.1016/S0896-6273(00)80173-7