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Citation
Tsuyama, T., Tsubouchi, A., Usui, T., Imamura, H., Uemura, T. (2017). Mitochondrial dysfunction induces dendritic loss via eIF2α phosphorylation.  J. Cell Biol. 216(3): 815--834.
FlyBase ID
FBrf0234947
Publication Type
Research paper
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.

PubMed ID
PubMed Central ID
PMC5346966 (PMC) (EuropePMC)
Related Publication(s)
Note

eIF2α links mitochondrial dysfunction to dendritic degeneration.
Qi, 2017, J. Cell Biol. 216(3): 555--557 [FBrf0235011]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    J. Cell Biol.
    Title
    Journal of Cell Biology
    Publication Year
    1966-
    ISBN/ISSN
    0021-9525
    Data From Reference