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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Courchet, Julien Lewis, Tommy L. Hellberg, Kristina Toyama, Erin Quan Herzig, Sébastien Young, Nathan P. Shaw, Reuben J. Losón, Oliver C. Chen, Hsiuchen Polleux, Franck Chan, David C. |
| Description | Author Affiliation: Toyama EQ ( Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.); Herzig S ( Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.); Courchet J ( Department of Neuroscience, Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, Columbia University, New York, NY 10032, USA.); Lewis TL ( Department of Neuroscience, Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, Columbia University, New York, NY 10032, USA.); Losón OC ( Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.); Hellberg K ( Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.); Young NP ( Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA.); Chen H ( Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.); Polleux F ( Department of Neuroscience, Zuckerman Mind Brain Behavior Institute and Kavli Institute for Brain Science, Columbia University, New York, NY 10032, USA.); Chan DC ( Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA.); Shaw RJ ( Molecular and Cell Biology Laboratory and Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, CA 92037, USA. shaw@salk.edu.) |
| Abstract | Mitochondria undergo fragmentation in response to electron transport chain (ETC) poisons and mitochondrial DNA-linked disease mutations, yet how these stimuli mechanistically connect to the mitochondrial fission and fusion machinery is poorly understood. We found that the energy-sensing adenosine monophosphate (AMP)-activated protein kinase (AMPK) is genetically required for cells to undergo rapid mitochondrial fragmentation after treatment with ETC inhibitors. Moreover, direct pharmacological activation of AMPK was sufficient to rapidly promote mitochondrial fragmentation even in the absence of mitochondrial stress. A screen for substrates of AMPK identified mitochondrial fission factor (MFF), a mitochondrial outer-membrane receptor for DRP1, the cytoplasmic guanosine triphosphatase that catalyzes mitochondrial fission. Nonphosphorylatable and phosphomimetic alleles of the AMPK sites in MFF revealed that it is a key effector of AMPK-mediated mitochondrial fission. |
| ISSN | 00368075 |
| e-ISSN | 10959203 |
| Journal | Science |
| Issue Number | 6270 |
| Volume Number | 351 |
| Language | English |
| Publisher | American Association for the Advancement of Science (United States) |
| Publisher Date | 2016-01-15 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | AMP-Activated Protein Kinases Metabolism Energy Metabolism Mitochondria Physiology Mitochondrial Dynamics Stress, Physiological Chemistry Genetics Adenosine Monophosphate Amino Acid Motifs Cell Line, Tumor Cytoplasm Enzymology Dactinomycin Analogs & Derivatives Pharmacology Enzyme Activation GTP Phosphohydrolases Microtubule-Associated Proteins Drug Effects Mitochondrial Proteins Molecular Sequence Data Rotenone Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | History and Philosophy of Science |
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