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@ARTICLE{Piazzesi:163786,
author = {Piazzesi, Antonia and Wang, Yiru and Jackson, Joshua and
Wischhof, Lena and Zeisler-Diehl, Viktoria and Scifo, Enzo
and Oganezova, Ina and Hoffmann, Nils Thorben and Gomez,
Pablo and Bertan, Fabio and Wrobel, Chester J J and
Schroeder, Frank C and Ehninger, Dan and Händler, Kristian
and Schultze, Joachim L and Schreiber, Lukas and
Echten-Deckert, Gerhild and Nicotera, Pierluigi and Bano,
Daniele},
title = {{CEST}‐2.2 overexpression alters lipid metabolism and
extends longevity of mitochondrial mutants},
journal = {EMBO reports},
volume = {23},
number = {5},
issn = {1469-221X},
address = {Hoboken, NJ [u.a.]},
publisher = {Wiley},
reportid = {DZNE-2022-00524},
pages = {e52606},
year = {2022},
abstract = {Mitochondrial dysfunction can either extend or decrease
Caenorhabditis elegans lifespan, depending on whether
transcriptionally regulated responses can elicit durable
stress adaptation to otherwise detrimental lesions. Here, we
test the hypothesis that enhanced metabolic flexibility is
sufficient to circumvent bioenergetic abnormalities
associated with the phenotypic threshold effect, thereby
transforming short-lived mitochondrial mutants into
long-lived ones. We find that CEST-2.2, a carboxylesterase
mainly localizes in the intestine, may stimulate the
survival of mitochondrial deficient animals. We report that
genetic manipulation of cest-2.2 expression has a minor
lifespan impact on wild-type nematodes, whereas its
overexpression markedly extends the lifespan of complex
I-deficient gas-1(fc21) mutants. We profile the
transcriptome and lipidome of cest-2.2 overexpressing
animals and show that CEST-2.2 stimulates lipid metabolism
and fatty acid beta-oxidation, thereby enhancing
mitochondrial respiratory capacity through complex II and
LET-721/ETFDH, despite the inherited genetic lesion of
complex I. Together, our findings unveil a metabolic pathway
that, through the tissue-specific mobilization of lipid
deposits, may influence the longevity of mitochondrial
mutant C. elegans.},
keywords = {Animals / Caenorhabditis elegans: metabolism /
Caenorhabditis elegans Proteins: genetics / Caenorhabditis
elegans Proteins: metabolism / Lipid Metabolism: genetics /
Longevity: genetics / Mitochondria: metabolism},
cin = {AG Bano / AG Ehninger / AG Schultze / $R\&D$ PRECISE /
Scientific board},
ddc = {570},
cid = {I:(DE-2719)1013003 / I:(DE-2719)1013005 /
I:(DE-2719)1013031 / I:(DE-2719)5000031 /
I:(DE-2719)1030000},
pnm = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
(POF4-352) / 354 - Disease Prevention and Healthy Aging
(POF4-354)},
pid = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
G:(DE-HGF)POF4-354},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC9066074},
pubmed = {pmid:35297148},
doi = {10.15252/embr.202152606},
url = {https://pub.dzne.de/record/163786},
}