Delayed-relaxed response explained by hyperactivation of RelE.

作者: Susanne K. Christensen , Kenn Gerdes

DOI: 10.1111/J.1365-2958.2004.04127.X

关键词:

摘要: Summary Escherichia coli encodes two rel loci, both of which contribute to the control synthesis macromolecules during amino acid starvation. The product relA (ppGpp synthetase I) is responsible for guanosine tetraphosphate, ppGpp, signal molecule that exerts stringent stable RNA synthesis. second locus, relBE, was identified by mutations in relB confer a so-called ‘delayed-relaxed response’ characterized continued after lag period ≈ 10 min onset We show here delayed-relaxed response consequence hyperactivation RelE. As wild-type cells, [ppGpp] increased sharply relB101 relE cells starvation, but returned rapidly prestarvation level. RelE global inhibitor translation neutralized RelB direct protein–protein interaction. Lon protease activates starvation degradation RelB. found conferred phenotype destabilized Such severe RelE-dependent inhibition indicating Hyperactivation shown directly measurement RelE-mediated cleavage tmRNA. shutdown terminated consumption and explains rapid restoration ppGpp level observed mutant cells. Restoration turn, allows resumption seen response.

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