ArticleThe Journal of cell biology2020
Mitochondrial translation and dynamics synergistically extend lifespan in C. elegans through HLH-30.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
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- Mitochondrial energy state controls AMPK-mediated foraging behavior inScience advances · 2024Article
- Combinatorial interventions in aging.Nature aging · 2023Review
- The mitochondrial calcium uniporter (MCU) activates mitochondrial respiration and enhances mobility by regulating mitochondrial redox state.Redox biology · 2023Article
- Reducing mitochondrial ribosomal gene expression does not alter metabolic health or lifespan in mice.Scientific reports · 2023Article
- Neuronal HLH-30/TFEB modulates peripheral mitochondrial fragmentation to improve thermoresistance in Caenorhabditis elegans.Aging cell · 2023Article
- MAVS Antagonizes Human Stem Cell Senescence as a Mitochondrial Stabilizer.Research (Washington, D.C.) · 2023Article
- Live or death in cells: from micronutrition metabolism to cell fate.Frontiers in cell and developmental biology · 2023Review
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- Crosstalk of organelles in Parkinson's disease - MiT family transcription factors as central players in signaling pathways connecting mitochondria and lysosomes.Molecular neurodegeneration · 2022Review
- Polar metabolomics in human muscle biopsies using a liquid-liquid extraction and full-scan LC-MS.STAR protocols · 2022Article
- Intestine-to-neuronal signaling alters risk-taking behaviors in food-deprived Caenorhabditis elegans.PLoS genetics · 2022Article
- Review
- Multi-omics analysis identifies essential regulators of mitochondrial stress response in two wild-typeiScience · 2022Article
- Insights Into the Links Between Proteostasis and Aging FromFrontiers in aging · 2022Review
- Targeting Mitochondrial Network Disorganization is Protective inAging and disease · 2021Article
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Mitochondrial form and function are closely interlinked in homeostasis and aging. Inhibiting mitochondrial translation is known to increase lifespan in C. elegans, and is accompanied by a fragmented mitochondrial network. However, whether this link between mitochondrial translation and morphology is causal in longevity remains uncharacterized. Here, we show in C. elegans that disrupting mitochondrial network homeostasis by blocking fission or fusion synergizes with reduced mitochondrial translation to prolong lifespan and stimulate stress response such as the mitochondrial unfolded protein response, UPRMT. Conversely, immobilizing the mitochondrial network through a simultaneous disruption of fission and fusion abrogates the lifespan increase induced by mitochondrial translation inhibition. Furthermore, we find that the synergistic effect of inhibiting both mitochondrial translation and dynamics on lifespan, despite stimulating UPRMT, does not require it. Instead, this lifespan-extending synergy is exclusively dependent on the lysosome biogenesis and autophagy transcription factor HLH-30/TFEB. Altogether, our study reveals the mechanistic crosstalk between mitochondrial translation, mitochondrial dynamics, and lysosomal signaling in regulating longevity.
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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.