Induction of BIM, a proapoptotic BH3-only BCL-2 family member, is critical for neuronal apoptosis

Neuron. 2001 Mar;29(3):615-28. doi: 10.1016/s0896-6273(01)00238-0.

Abstract

Sympathetic neuronal death induced by nerve growth factor (NGF) deprivation requires the macromolecular synthesis-dependent translocation of BAX from the cytosol to mitochondria and its subsequent integration into the mitochondrial outer membrane, followed by BAX-mediated cytochrome c (cyt c) release. The gene products triggering this process remain unknown. Here, we report that BIM, a member of the BH3-only proapoptotic subfamily of the BCL-2 protein family, is one such molecule. NGF withdrawal induced expression of BIM(EL), an integral mitochondrial membrane protein that functions upstream of (or in parallel with) the BAX/BCL-2 and caspase checkpoints. Bim deletion conferred protection against developmental and induced neuronal apoptosis in both central and peripheral populations, but only transiently, suggesting that BIM--and perhaps other BH3-only proteins--serve partially redundant functions upstream of BAX-mediated cyt c release.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alternative Splicing
  • Animals
  • Animals, Newborn
  • Apoptosis / physiology*
  • Apoptosis Regulatory Proteins
  • Bcl-2-Like Protein 11
  • Carrier Proteins / biosynthesis*
  • Carrier Proteins / genetics
  • Carrier Proteins / physiology
  • Caspases / metabolism
  • Cells, Cultured
  • Cycloheximide / pharmacology
  • Cytochrome c Group / metabolism
  • Cytosol / metabolism
  • Dactinomycin / pharmacology
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Intracellular Membranes / metabolism
  • JNK Mitogen-Activated Protein Kinases*
  • MAP Kinase Kinase 4
  • Membrane Proteins*
  • Mice
  • Mitochondria / metabolism
  • Mitochondria / ultrastructure
  • Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase Kinases / physiology
  • Mutagenesis
  • Nerve Growth Factor / administration & dosage
  • Nerve Growth Factor / physiology
  • Neurons / physiology*
  • Neurons / ultrastructure
  • Phosphatidylinositol 3-Kinases / physiology
  • Phosphoinositide-3 Kinase Inhibitors
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • RNA, Messenger / analysis
  • Rats
  • Reverse Transcriptase Polymerase Chain Reaction
  • bcl-2-Associated X Protein

Substances

  • Apoptosis Regulatory Proteins
  • Bax protein, mouse
  • Bax protein, rat
  • Bcl-2-Like Protein 11
  • Bcl2l11 protein, mouse
  • Bcl2l11 protein, rat
  • Carrier Proteins
  • Cytochrome c Group
  • Enzyme Inhibitors
  • Membrane Proteins
  • Phosphoinositide-3 Kinase Inhibitors
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • bcl-2-Associated X Protein
  • Dactinomycin
  • Nerve Growth Factor
  • Cycloheximide
  • JNK Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase 4
  • Mitogen-Activated Protein Kinase Kinases
  • Caspases