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dc.contributor.author
Liu, Yasmine J.
dc.contributor.author
McIntyre, Rebecca L.
dc.contributor.author
Janssens, Georges E.
dc.contributor.author
Williams, Evan G.
dc.contributor.author
Lan, Jiayi
dc.contributor.author
van Weeghel, Michel
dc.contributor.author
Schomakers, Bauke
dc.contributor.author
van der Veen, Henk
dc.contributor.author
van der Wel, Nicole N.
dc.contributor.author
Yao, Pallas
dc.contributor.author
Mair, William B.
dc.contributor.author
Aebersold, Ruedi
dc.contributor.author
MacInnes, Alyson W.
dc.contributor.author
Houtkooper, Riekelt H.
dc.date.accessioned
2020-04-17T10:42:22Z
dc.date.available
2020-04-17T09:57:59Z
dc.date.available
2020-04-17T10:42:22Z
dc.date.issued
2020-06-01
dc.identifier.issn
0021-9525
dc.identifier.issn
1540-8140
dc.identifier.other
10.1083/jcb.201907067
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/410324
dc.identifier.doi
10.3929/ethz-b-000410324
dc.description.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.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Rockefeller University Press
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc-sa/4.0/
dc.title
Mitochondrial translation and dynamics synergistically extend lifespan in C. elegans through HLH-30
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International
dc.date.published
2020-04-07
ethz.journal.title
The Journal of Cell Biology
ethz.journal.volume
219
en_US
ethz.journal.issue
6
en_US
ethz.journal.abbreviated
J. Cell Biol.
ethz.pages.start
e201907067
en_US
ethz.size
27 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
New York, NY
en_US
ethz.publication.status
published
en_US
ethz.date.deposited
2020-04-17T09:58:01Z
ethz.source
SCOPUS
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2020-04-17T10:42:43Z
ethz.rosetta.lastUpdated
2020-04-17T10:42:43Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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