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    The mitochondrial fission protein hFis1 requires the endoplasmic reticulum gateway to induce apoptosis.

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    Authors
    Alirol, Emilie
    James, Dominic I
    Huber, Denise
    Marchetto, Andrea
    Vergani, Lodovica
    Martinou, Jean-Claude
    Scorrano, Luca
    Affiliation
    Dulbecco-Telethon Institute, Venetian Institute of Molecular Medicine, I-35129 Padova, Italy.
    Issue Date
    2006-11
    
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    Abstract
    Mitochondrial fission ensures organelle inheritance during cell division and participates in apoptosis. The fission protein hFis1 triggers caspase-dependent cell death, by causing the release of cytochrome c from mitochondria. Here we show that mitochondrial fission induced by hFis1 is genetically distinct from apoptosis. In cells lacking the multidomain proapoptotic Bcl-2 family members Bax and Bak (DKO), hFis1 caused mitochondrial fragmentation but not organelle dysfunction and apoptosis. Similarly, a mutant in the intermembrane region of hFis1-induced fission but not cell death, further dissociating mitochondrial fragmentation from apoptosis induction. Selective correction of the endoplasmic reticulum (ER) defect of DKO cells restored killing by hFis1, indicating that death by hFis1 relies on the ER gateway of apoptosis. Consistently, hFis1 did not directly activate BAX and BAK, but induced Ca(2+)-dependent mitochondrial dysfunction. Thus, hFis1 is a bifunctional protein that independently regulates mitochondrial fragmentation and ER-mediated apoptosis.
    Citation
    The mitochondrial fission protein hFis1 requires the endoplasmic reticulum gateway to induce apoptosis. 2006, 17 (11):4593-605 Mol. Biol. Cell
    Journal
    Molecular Biology of the Cell
    URI
    http://hdl.handle.net/10541/72773
    DOI
    10.1091/mbc.E06-05-0377
    PubMed ID
    16914522
    Type
    Article
    Language
    en
    ISSN
    1059-1524
    ae974a485f413a2113503eed53cd6c53
    10.1091/mbc.E06-05-0377
    Scopus Count
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    All Paterson Institute for Cancer Research

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