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Related Experiment Videos

Delayed-relaxed response explained by hyperactivation of RelE.

Susanne K Christensen1, Kenn Gerdes

  • 1Department of Biochemistry and Molecular Biology, University of Southern Denmark, DK-5230 Odense M, Denmark.

Molecular Microbiology
|July 2, 2004
PubMed
Summary

Escherichia coli uses two rel loci to control macromolecule synthesis during starvation. Mutations in relB lead to hyperactivation of RelE, a translation inhibitor, causing a delayed-relaxed response.

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Bacterial Physiology

Background:

  • Escherichia coli possesses two rel loci involved in regulating macromolecule synthesis under amino acid starvation.
  • RelA produces guanosine tetraphosphate (ppGpp), a key signal molecule for stringent control of stable RNA synthesis.
  • Mutations in relB can cause a 'delayed-relaxed response,' characterized by a temporary halt in RNA synthesis after starvation onset.

Purpose of the Study:

  • To elucidate the molecular mechanism behind the 'delayed-relaxed response' in Escherichia coli.
  • To investigate the role of the relBE locus and the interaction between RelB and RelE in bacterial stress response.

Main Methods:

  • Genetic analysis of relB mutations and their effect on the delayed-relaxed response.
  • Biochemical assays to measure ppGpp levels and RelE activity.

Related Experiment Videos

  • Protein-protein interaction studies between RelB and RelE.
  • Analysis of tmRNA cleavage to assess RelE-mediated translation inhibition.

    • Main Results:

    • The delayed-relaxed response is caused by hyperactivation of the RelE translation inhibitor.
    • RelB normally neutralizes RelE activity through direct protein-protein interaction.
    • Lon protease degrades RelB during starvation, activating RelE.
    • Mutations in relB destabilize RelB, leading to uncontrolled RelE activation and severe translation inhibition.

    Conclusions:

    • RelE acts as a global translation inhibitor, tightly regulated by RelB.
    • Starvation-induced degradation of RelB by Lon protease leads to RelE hyperactivation.
    • This hyperactivation causes a temporary shutdown of translation, reducing amino acid consumption and allowing ppGpp levels to return to normal.
    • The restoration of ppGpp enables the resumption of stable RNA synthesis, explaining the delayed-relaxed phenotype.