4.6 Article

Glucose starvation induces mitochondrial fragmentation depending on the dynamin GTPase Dnm1/Drp1 in fission yeast

Journal

JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 294, Issue 47, Pages 17725-17734

Publisher

AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.RA119.010185

Keywords

mitochondria; stress; glucose; dynamin; fungi

Funding

  1. National Key Research and Development Program of China [2018YFC1004700]
  2. National Natural Science Foundation of China [91754106, 31871350, 31671406, 31601095, 31621002]
  3. Strategic Priority Research Program of the Chinese Academy of Sciences Grant [XDB19040101]
  4. Major/Innovative Program of Development Foundation of the Hefei Center for Physical Science and Technology [2017FXCX008]
  5. China's 1000 Young Talents Recruitment Program

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Mitochondria undergo morphological and dynamic changes in response to environmental stresses. Few studies have focused on addressing mitochondrial remodeling under stress. Using the fission yeast Schizosaccharomyces pombe as a model organism, here we investigated mitochondrial remodeling under glucose starvation. We employed live-cell microscopy to monitor mitochondrial morphology and dynamics of cells in profusion chambers under glucose starvation. Our results revealed that mitochondria fragment within minutes after glucose starvation and that the dynamin GTPase Dnm1 is required for promoting mitochondrial fragmentation. Moreover, we found that glucose starvation enhances Dnm1 localization to mitochondria and increases the frequency of mitochondrial fission but decreases PKA activity. We further demonstrate that low PKA activity enhances glucose starvation?induced mitochondrial fragmentation, whereas high PKA activity confers resistance to glucose starvation?induced mitochondrial fragmentation. Moreover, we observed that AMP-activated protein kinase is not involved in regulating mitochondrial fragmentation under glucose starvation. Of note, glucose starvation?induced mitochondrial fragmentation was associated with enhanced reactive oxygen species production. Our work provides detailed mechanistic insights into mitochondrial remodeling in response to glucose starvation.

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