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We are analyzing https://www.nature.com/articles/s41467-017-00274-4.

Title:
Increased mitochondrial fusion allows the survival of older animals in diverse C. elegans longevity pathways | Nature Communications
Description:
Mitochondria are dynamic organelles that undergo fusion and fission events. Mitochondrial dynamics are required for mitochondrial viability and for responses to changes in bioenergetic status. Here we describe an insulin-signaling and SCFLIN-23-regulated pathway that controls mitochondrial fusion in Caenorhabditis elegans by repressing the expression of the mitochondrial proteases SPG-7 and PPGN-1. This pathway is required for mitochondrial fusion in response to physical exertion, and for the associated extension in lifespan. We show that diverse longevity pathways exhibit increased levels of elongated mitochondria. The increased mitochondrial fusion is essential for longevity in the diverse longevity pathways, as inhibiting mitochondrial fusion reduces their lifespans to wild-type levels. Our results suggest that increased mitochondrial fusion is not a major driver of longevity, but rather is essential to allow the survival of older animals beyond their normal lifespan in diverse longevity pathways. Mitochondria can undergo shape changes as a result of fusion and fission events. Here the authors describe how insulin signalling regulates mitochondrial fusion in C. elegans, and show that mitochondrial fusion is necessary, but not sufficient, for longevity of worms with mutations that increase lifespan.
Website Age:
30 years and 10 months (reg. 1994-08-11).

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  • Science
  • Fitness & Wellness
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Custom-built

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πŸŒ† Monumental Traffic: 20M - 50M visitors per month


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Keywords {πŸ”}

mitochondrial, pubmed, fig, animals, lifespan, article, fusion, mitochondria, levels, cand, rnai, google, scholar, mutants, increased, cas, elegans, spg, elongated, daf, supplementary, eat, cells, ppgn, central, pathway, protein, longevity, swimming, cell, muscle, expression, spgek, akt, control, plates, swim, nature, atp, increase, denote, morphology, lin, extension, wildtype, analyzed, survival, required, significantly, uprmt,

Topics {βœ’οΈ}

nature portfolio research infrastructure programs privacy policy elegans research community l4/young-adult-stage animals treated 1 mm isopropyl Ξ²-d-1-thiogalactopyranoside 5 mm n-nitroso-n-ethylurea advertising l4/young-adult-stage animals liquid 2xyt media dynamin-related protein dnml1 mitochondrial m-aaa protease l4/young-adult stage reprints nature 521 nature nature 366 dynamin-related protein drp-1 cullin-ring ubiquitin ligase cullin-ring ubiquitin ligases late-l4-stage larvae body-wall muscle cells59 late-l4 larval stage young-adult-stage animals detect k63 poly-ubiquitin body-wall muscle cells elegans body-wall muscles rnase/dnase-free water eat-3/opa1-dependent mitochondrial fusion author information authors m-aaa protease social media real-time pcr quantification increased atp/protein ratios tissue-specific subunit composition daf-2-mediated development org/chapters/www_insulingrowthsignal/insulingrowthsignal elegans insulin/igf-1 signaling detects akt-phosphorylated substrates prior larval development recognizes akt phospho-substrates cop9/signalosome component csn-3 k63-linked poly-ubiquitylation activate daf-16-mediated repression anti-histone h4 staining permissions long-lived mutants/rnai animals mitochondrial import efficiency consensus daf-16-binding element hypoxia-inducible factor hif1Ξ±

Schema {πŸ—ΊοΈ}

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         description:Mitochondria are dynamic organelles that undergo fusion and fission events. Mitochondrial dynamics are required for mitochondrial viability and for responses to changes in bioenergetic status. Here we describe an insulin-signaling and SCFLIN-23-regulated pathway that controls mitochondrial fusion in Caenorhabditis elegans by repressing the expression of the mitochondrial proteases SPG-7 and PPGN-1. This pathway is required for mitochondrial fusion in response to physical exertion, and for the associated extension in lifespan. We show that diverse longevity pathways exhibit increased levels of elongated mitochondria. The increased mitochondrial fusion is essential for longevity in the diverse longevity pathways, as inhibiting mitochondrial fusion reduces their lifespans to wild-type levels. Our results suggest that increased mitochondrial fusion is not a major driver of longevity, but rather is essential to allow the survival of older animals beyond their normal lifespan in diverse longevity pathways. Mitochondria can undergo shape changes as a result of fusion and fission events. Here the authors describe how insulin signalling regulates mitochondrial fusion in C. elegans, and show that mitochondrial fusion is necessary, but not sufficient, for longevity of worms with mutations that increase lifespan.
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      headline:Increased mitochondrial fusion allows the survival of older animals in diverse C. elegans longevity pathways
      description:Mitochondria are dynamic organelles that undergo fusion and fission events. Mitochondrial dynamics are required for mitochondrial viability and for responses to changes in bioenergetic status. Here we describe an insulin-signaling and SCFLIN-23-regulated pathway that controls mitochondrial fusion in Caenorhabditis elegans by repressing the expression of the mitochondrial proteases SPG-7 and PPGN-1. This pathway is required for mitochondrial fusion in response to physical exertion, and for the associated extension in lifespan. We show that diverse longevity pathways exhibit increased levels of elongated mitochondria. The increased mitochondrial fusion is essential for longevity in the diverse longevity pathways, as inhibiting mitochondrial fusion reduces their lifespans to wild-type levels. Our results suggest that increased mitochondrial fusion is not a major driver of longevity, but rather is essential to allow the survival of older animals beyond their normal lifespan in diverse longevity pathways. Mitochondria can undergo shape changes as a result of fusion and fission events. Here the authors describe how insulin signalling regulates mitochondrial fusion in C. elegans, and show that mitochondrial fusion is necessary, but not sufficient, for longevity of worms with mutations that increase lifespan.
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