E. coli hypoxia-inducible factor ArcA mediates lifespan extension in a lipoic acid synthase mutant by suppressing acetyl-CoA synthetase
-
Stavros Gonidakis
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.
©2010 by Walter de Gruyter Berlin New York
Articles in the same Issue
- Guest Editorial
- Highlight: The Biology of Aging: Mechanisms and Intervention
- Highlight: 61th Mosbach Colloquium of the GBM ‘The Biology of Aging: Mechanisms and Intervention’
- Multiplex analysis of mitochondrial DNA pathogenic and polymorphic sequence variants
- The hypoxia-inducible factor HIF-1 functions as both a positive and negative modulator of aging
- E. coli hypoxia-inducible factor ArcA mediates lifespan extension in a lipoic acid synthase mutant by suppressing acetyl-CoA synthetase
- Glucose homeostasis and insulin sensitivity in growth hormone-transgenic mice: a cross-sectional analysis
- PROTEIN STRUCTURE AND FUNCTION
- New structural aspects of FKBP38 activation
- The neuronal proteins CIPP, Cypin and IRSp53 form a tripartite complex mediated by PDZ and SH3 domains
- CELL BIOLOGY AND SIGNALING
- Inhibition of interferon-α-induced signaling by hyperosmolarity and hydrophobic bile acids
- Role of the second disulfide bridge (Cys18-Cys274) in stabilizing the inactive AT1 receptor
- Demonstration of protein absorption in the intestinal epithelium of fish and mice by laser scanning confocal microscopy
- Non-genomic action of TCDD to induce inflammatory responses in HepG2 human hepatoma cells and in liver of C57BL/6J mice
- PROTEOLYSIS
- Amino acid residues modulating the activities of staphylococcal glutamyl endopeptidases
Articles in the same Issue
- Guest Editorial
- Highlight: The Biology of Aging: Mechanisms and Intervention
- Highlight: 61th Mosbach Colloquium of the GBM ‘The Biology of Aging: Mechanisms and Intervention’
- Multiplex analysis of mitochondrial DNA pathogenic and polymorphic sequence variants
- The hypoxia-inducible factor HIF-1 functions as both a positive and negative modulator of aging
- E. coli hypoxia-inducible factor ArcA mediates lifespan extension in a lipoic acid synthase mutant by suppressing acetyl-CoA synthetase
- Glucose homeostasis and insulin sensitivity in growth hormone-transgenic mice: a cross-sectional analysis
- PROTEIN STRUCTURE AND FUNCTION
- New structural aspects of FKBP38 activation
- The neuronal proteins CIPP, Cypin and IRSp53 form a tripartite complex mediated by PDZ and SH3 domains
- CELL BIOLOGY AND SIGNALING
- Inhibition of interferon-α-induced signaling by hyperosmolarity and hydrophobic bile acids
- Role of the second disulfide bridge (Cys18-Cys274) in stabilizing the inactive AT1 receptor
- Demonstration of protein absorption in the intestinal epithelium of fish and mice by laser scanning confocal microscopy
- Non-genomic action of TCDD to induce inflammatory responses in HepG2 human hepatoma cells and in liver of C57BL/6J mice
- PROTEOLYSIS
- Amino acid residues modulating the activities of staphylococcal glutamyl endopeptidases
