Authors: Zhongyan Zhang, Yusuke Kageyama and Hiromi Sesaki

Zhongyan Zhang

Department of Cell Biology; Johns Hopkins University School of Medicine; Baltimore, MD USA

Yusuke Kageyama

Department of Cell Biology; Johns Hopkins University School of Medicine; Baltimore, MD USA

Hiromi Sesaki

Corresponding author: hsesaki@jhmi.edu
Department of Cell Biology; Johns Hopkins University School of Medicine; Baltimore, MD USA

Abstract:
Mitochondrial division is mediated by the conserved dynamin-related GTPase DNM1L/DRP1. DNM1L assembles onto the surface of mitochondria and constricts this tubular organelle. Alterations in mitochondrial division are linked to many neurodegenerative diseases. However, the in vivo function of mitochondrial division is poorly understood. In our recent paper, we studied the physiological role of mitochondrial division in postmitotic neurons using the cre-loxP system. We found that the loss of DNM1L resulted in increased oxidative damage in mitochondria, impaired respiration and neurodegeneration in postmitotic neurons. Suggesting a decrease in mitochondrial turnover, mitophagy-related proteins such as LC3, SQSTM1/p62 and ubiqutin accumulated in division-defective mitochondria. These findings suggest that mitochondrial division functions as an important quality control mechanism that suppresses oxidative damage and neurodegeneration in vivo

Autophagic Punctum to:
Y Kageyama, Z Zhang, R Roda, M Fukaya, J Wakabayashi, N Wakabayashi, et al. Mitochondrial division ensures the survival of postmitotic neurons by suppressing oxidative damage. J Cell Biol 2012; 197: 535-51
PMID: 22564413 DOI: 10.1083/jcb.201110034

Received: June 11, 2012; Accepted: June 21, 2012; Published Online: June 26, 2012

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