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All fields Title Creator / Publisher Keyword Year AND OR AND NOT All fields Title Creator / Publisher Keyword Year AND OR AND NOT All fields Title Creator / Publisher Keyword Year AND OR AND NOT All fields Title Creator / Publisher Keyword Year AND OR AND NOT All fields Title Creator / Publisher Keyword Year Sort by creator [A → Z]' creator [Z → A]' publishing year ↑ (asc)' publishing year ↓ (desc)' title [A → Z]' title [Z → A]' Simple Search Hits 1 – 2 of 2 1 Mitochondrial translation and dynamics synergistically extend lifespan in C. elegans through HLH-30 Liu, Yasmine J.; McIntyre, Rebecca L.; Janssens, Georges E.... In: The Journal of Cell Biology, 219 (6) (2020) BASE Show details 2 Mitochondrial translation and dynamics synergistically extend lifespan in C. elegans through HLH-30 Liu, Yasmine J.; McIntyre, Rebecca L.; Janssens, Georges E.; Williams, Evan G.; Lan, Jiayi; van Weeghel, Michel; Schomakers, Bauke; van der Veen, Henk; van der Wel, Nicole N.; Yao, Pallas; Mair, William B.; Aebersold, Ruedi; MacInnes, Alyson W.; Houtkooper, Riekelt H. In: J Cell Biol (2020) 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, UPR(MT). 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 UPR(MT), 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. Keyword: Article URL: https://doi.org/10.1083/jcb.201907067 http://www.ncbi.nlm.nih.gov/pubmed/32259199 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7265311/ BASE Hide details

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