Document Detail


Bcl-2 family interaction with the mitochondrial morphogenesis machinery.
MedLine Citation:
PMID:  20671748     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The regulation of both mitochondrial dynamics and apoptosis is key for maintaining the health of a cell. Bcl-2 family proteins, central in apoptosis regulation, also have roles in the maintenance of the mitochondrial network. Here we report that Bax and Bak participate in the regulation of mitochondrial fusion in mouse embryonic fibroblasts, primary mouse neurons and human colon carcinoma cells. To assess how Bcl-2 family members may regulate mitochondrial morphogenesis, we determined the binding of a series of chimeras between Bcl-xL and Bax to the mitofusins, mitofusin 1 (Mfn1) and mitofusin 2 (Mfn2). One chimera (containing helix 5 (H5) of Bax replacing H5 of Bcl-xL (Bcl-xL/Bax H5)) co-immunoprecipitated with Mfn1 and Mfn2 significantly better than either wild-type Bax or Bcl-xL. Expression of Bcl-xL/Bax H5 in cells reduced the mobility of Mfn1 and Mfn2 and colocalized with ectopic Mfn1 and Mfn2, as well as endogenous Mfn2 to a greater extent than wild-type Bax. Ultimately, Bcl-xL/Bax H5 induced substantial mitochondrial fragmentation in healthy cells. Therefore, we propose that Bcl-xL/Bax H5 disturbs mitochondrial morphology by binding and inhibiting Mfn1 and Mfn2 activity, supporting the hypothesis that Bcl-2 family members have the capacity to regulate mitochondrial morphology through binding to the mitofusins in healthy cells.
Authors:
M M Cleland; K L Norris; M Karbowski; C Wang; D-F Suen; S Jiao; N M George; X Luo; Z Li; R J Youle
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural     Date:  2010-07-30
Journal Detail:
Title:  Cell death and differentiation     Volume:  18     ISSN:  1476-5403     ISO Abbreviation:  Cell Death Differ.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-10     Completed Date:  2011-04-25     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  9437445     Medline TA:  Cell Death Differ     Country:  England    
Other Details:
Languages:  eng     Pagination:  235-47     Citation Subset:  IM    
Affiliation:
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Cell Line
Fibroblasts / metabolism
GTP Phosphohydrolases / genetics,  metabolism
Humans
Immunoprecipitation
Mice
Mitochondria / metabolism*,  ultrastructure
Neurons / metabolism
Protein Structure, Tertiary
Proto-Oncogene Proteins c-bcl-2 / metabolism*
bcl-2 Homologous Antagonist-Killer Protein / genetics,  metabolism
bcl-2-Associated X Protein / genetics,  metabolism
bcl-X Protein / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
R01 GM076237-05/GM/NIGMS NIH HHS; R01 GM083131-01A1/GM/NIGMS NIH HHS; R01-GM083131/GM/NIGMS NIH HHS; R01-GM76237/GM/NIGMS NIH HHS; Z01 MH002881-01/MH/NIMH NIH HHS; Z01 NS002859-17/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2 Homologous Antagonist-Killer Protein; 0/bcl-2-Associated X Protein; 0/bcl-X Protein; EC 3.6.1.-/GTP Phosphohydrolases; EC 3.6.1.-/Mfn1 protein, mouse; EC 3.6.1.-/Mfn2 protein, mouse
Comments/Corrections

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