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PLoS One. 2016 Apr 11;11(4):e0153233. doi: 10.1371/journal.pone.0153233. eCollection 2016.

C. elegans miro-1 Mutation Reduces the Amount of Mitochondria and Extends Life Span.

Author information

1
Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
2
Science Division, Yale-NUS College, Singapore, Singapore.

Abstract

Mitochondria play a critical role in aging, however, the underlying mechanism is not well understood. We found that a mutation disrupting the C. elegans homolog of Miro GTPase (miro-1) extends life span. This phenotype requires simultaneous loss of miro-1 from multiple tissues including muscles and neurons, and is dependent on daf-16/FOXO. Notably, the amount of mitochondria in the miro-1 mutant is reduced to approximately 50% of the wild-type. Despite this reduction, oxygen consumption is only weakly reduced, suggesting that mitochondria of miro-1 mutants are more active than wild-type mitochondria. The ROS damage is slightly reduced and the mitochondrial unfolded protein response pathway is weakly activated in miro-1 mutants. Unlike previously described long-lived mitochondrial electron transport chain mutants, miro-1 mutants have normal growth rate. These results suggest that the reduction in the amount of mitochondria can affect the life span of an organism through activation of stress pathways.

PMID:
27064409
PMCID:
PMC4827821
DOI:
10.1371/journal.pone.0153233
[Indexed for MEDLINE]
Free PMC Article

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