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Title: Mitochondrial dysfunction induces dendritic loss via eIF2α phosphorylation
Authors: Tsuyama, Taiichi
Tsubouchi, Asako
Usui, Tadao  kyouindb  KAKEN_id  orcid (unconfirmed)
Imamura, Hiromi  kyouindb  KAKEN_id  orcid (unconfirmed)
Uemura, Tadashi  kyouindb  KAKEN_id  orcid (unconfirmed)
Author's alias: 津山, 泰一
坪内, 朝子
碓井, 理夫
今村, 博臣
上村, 匡
Issue Date: Mar-2017
Publisher: Rockefeller University Press
Journal title: Journal of Cell Biology
Volume: 216
Issue: 3
Start page: 815
End page: 834
Abstract: Mitochondria are key contributors to the etiology of diseases associated with neuromuscular defects or neurodegeneration. How changes in cellular metabolism specifically impact neuronal intracellular processes and cause neuropathological events is still unclear. We here dissect the molecular mechanism by which mitochondrial dysfunction induced by Prel aberrant function mediates selective dendritic loss in Drosophila melanogaster class IV dendritic arborization neurons. Using in vivo ATP imaging, we found that neuronal cellular ATP levels during development are not correlated with the progression of dendritic loss. We searched for mitochondrial stress signaling pathways that induce dendritic loss and found that mitochondrial dysfunction is associated with increased eIF2α phosphorylation, which is sufficient to induce dendritic pathology in class IV arborization neurons. We also observed that eIF2α phosphorylation mediates dendritic loss when mitochondrial dysfunction results from other genetic perturbations. Furthermore, mitochondrial dysfunction induces translation repression in class IV neurons in an eIF2α phosphorylation-dependent manner, suggesting that differential translation attenuation among neuron subtypes is a determinant of preferential vulnerability.
Rights: © 2017 Tsuyama et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at
DOI(Published Version): 10.1083/jcb.201604065
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