Bcl-x L increases mitochondrial fission, fusion, and biomass in neurons

Sarah B. Berman, Ying Bei Chen, Bing Qi, J. Michael McCaffery, Edmund B. Rucker, Sandra Goebbels, Klaus Armin Nave, Beth A. Arnold, Elizabeth A. Jonas, Fernando J. Pineda, J. Marie Hardwick

Research output: Contribution to journalArticlepeer-review

158 Scopus citations


Mitochondrial fi ssion and fusion are linked to synaptic activity in healthy neurons and are implicated in the regulation of apoptotic cell death in many cell types. We developed fl uorescence microscopy and computational strategies to directly measure mitochondrial fission and fusion frequencies and their effects on mitochondrial morphology in cultured neurons. We found that the rate of fission exceeds the rate of fusion in healthy neuronal processes, and, therefore, the fission/fusion ratio alone is insufficient to explain mitochondrial morphology at steady state. This imbalance between fission and fusion is compensated by growth of mitochondrial organelles. Bcl-x L increases the rates of both fusion and fission, but more important for explaining the longer organelle morphology induced by Bcl-x L is its ability to increase mitochondrial biomass. Deficits in these Bcl-x L - dependent mechanisms may be critical in neuronal dysfunction during the earliest phases of neurodegeneration, long before commitment to cell death.

Original languageEnglish (US)
Pages (from-to)707-719
Number of pages13
JournalJournal of Cell Biology
Issue number5
StatePublished - Mar 9 2009

ASJC Scopus subject areas

  • Cell Biology


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