論文

査読有り
2016年3月

Mitochondrial fission protein Drp1 regulates mitochondrial transport and dendritic arborization in cerebellar Purkinje cells

MOLECULAR AND CELLULAR NEUROSCIENCE
  • Kansai Fukumitsu
  • ,
  • Tetsu Hatsukano
  • ,
  • Azumi Yoshimura
  • ,
  • John Heuser
  • ,
  • Kazuto Fujishima
  • ,
  • Mineko Kengaku

71
開始ページ
56
終了ページ
65
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.mcn.2015.12.006
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Mitochondria dynamically change their shape by repeated fission and fusion in response to physiological and pathological conditions. Recent studies have uncovered significant roles of mitochondrial fission and fusion in neuronal functions, such as neurotransmission and spine formation. However, the contribution of mitochondrial fission to the development of dendrites remains controversial. We analyzed the function of the mitochondrial fission GTPase Drp1 in dendritic arborization in cerebellar Purkinje cells. Overexpression of a dominant-negative mutant of Drp1 in postmitotic Purkinje cells enlarged and clustered mitochondria, which failed to exit from the soma into the dendrites. The emerging dendrites lacking mitochondrial transport remained short and unstable in culture and in vivo. The dominant-negative Drp1 affected neither the basal respiratory function of mitochondria nor the survival of Purkinje cells. Enhanced ATP supply by creatine treatment, but not reduced ROS production by antioxidant treatment, restored the hypomorphic dendrites caused by inhibition of Drp1 function. Collectively, our results suggest that Drp1 is required for dendritic distribution of mitochondria and thereby regulates energy supply in growing dendritic branches in developing Purkinje cells. (C) 2015 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.mcn.2015.12.006
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000371443900006&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.mcn.2015.12.006
  • ISSN : 1044-7431
  • eISSN : 1095-9327
  • Web of Science ID : WOS:000371443900006

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