ArticlePloS one2016
C. elegans miro-1 Mutation Reduces the Amount of Mitochondria and Extends Life Span.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed.
- Ultrastructural Analysis Reveals Mitochondrial Placement Independent of Synapse Placement in Fine Caliber C. elegans Neurons.The Journal of comparative neurology · 2024Article
- Review
- Structural regulation and dynamic behaviour of organelles during plant meiosis.Frontiers in cell and developmental biology · 2022Review
- Metaxins are core components of mitochondrial transport adaptor complexes.Nature communications · 2021Article
- Drp-1-Dependent Mitochondrial Fragmentation Contributes to Cobalt Chloride-Induced Toxicity in Caenorhabditis elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Binucleate germ cells in Caenorhabditis elegans are removed by physiological apoptosis.PLoS genetics · 2018Article
- UNC-16/JIP3 and UNC-76/FEZ1 limit the density of mitochondria in C. elegans neurons by maintaining the balance of anterograde and retrograde mitochondrial transport.Scientific reports · 2018Article
- Cell Biology of the Mitochondrion.Genetics · 2017Review
- Of yeast, mice and men: MAMs come in two flavors.Biology direct · 2017Review
- A Select Subset of Electron Transport Chain Genes Associated with Optic Atrophy Link Mitochondria to Axon Regeneration inFrontiers in neuroscience · 2017Article
- Review
Corrections and comments
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Authors and funding
6 authors.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.