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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred


IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

Online
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1437-4315
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Volume 391, Issue 10

Issues

E. coli hypoxia-inducible factor ArcA mediates lifespan extension in a lipoic acid synthase mutant by suppressing acetyl-CoA synthetase

Stavros Gonidakis
  • Integrative and Evolutionary Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Steven E. Finkel
  • Molecular and Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Valter D. Longo
  • Andrus Gerontology Center, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2010-08-13 | DOI: https://doi.org/10.1515/bc.2010.120

Abstract

We have previously shown that both the hypoxia-inducible transcription factor ArcA and the PoxB/Acs bypass of the pyruvate dehydrogenase complex contribute to extended lifespan in Escherichia coli. In agreement with studies in higher eukaryotes, we also demonstrated that long-lived E. coli mutants, including LipA-deficient cells, are stress resistant. Here, we show that ArcA contributes to the enhanced lifespan and heat shock resistance of the lipA mutant by suppressing expression of the acetyl-CoA synthetase (acs) gene. The deletion of acs reversed the reduced lifespan of the lipA arcA mutant and promoted the accumulation of extracellular acetate, indicating that inhibition of carbon source uptake contributes to survival extension. However, Acs also sensitized cells lacking ArcA to heat shock, in the absence of extracellular acetate. These results provide evidence for the role of Acs in regulating lifespan and/or stress resistance by both carbon source uptake-dependent and -independent mechanisms.

Keywords: acetate; ATP; heat shock resistance; oxygen consumption; protein carbonylation

About the article

Corresponding author


Received: 2010-05-19

Accepted: 2010-06-30

Published Online: 2010-08-13

Published in Print: 2010-10-01


Citation Information: Biological Chemistry, Volume 391, Issue 10, Pages 1139–1147, ISSN (Online) 1437-4315, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/bc.2010.120.

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