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Related Experiment Videos

The SOS response regulates adaptive mutation.

G J McKenzie1, R S Harris, P L Lee

  • 1Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

Proceedings of the National Academy of Sciences of the United States of America
|June 1, 2000
PubMed
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Escherichia coli cells use adaptive mutation, a genome-wide hypermutation during starvation, to generate genetic variability. This stress response is tightly regulated by the SOS system, involving both positive and negative controls.

Area of Science:

  • Microbiology
  • Genetics
  • Molecular Biology

Background:

  • Escherichia coli exhibits adaptive mutation, a transient genome-wide hypermutation, under starvation stress.
  • This recombination-dependent process is thought to generate genetic variability in response to environmental challenges.
  • The regulatory mechanisms and signal transduction pathways governing adaptive mutation were previously unknown.

Purpose of the Study:

  • To elucidate the regulatory components and signal transduction pathways controlling adaptive mutation in Escherichia coli.
  • To investigate the role of the SOS response in adaptive mutation.

Main Methods:

  • Investigated the role of the SOS response in adaptive mutation.
  • Assessed the requirement of specific proteins, including RecF, for efficient adaptive mutation.

Related Experiment Videos

  • Identified SOS-controlled regulators of adaptive mutation.

    • Main Results:

    • Adaptive mutation is regulated by the SOS response, a DNA damage-induced pathway.
    • SOS-induced proteins, beyond RecA, are necessary for adaptive mutation.
    • RecF is required for efficient adaptive mutation, potentially by facilitating SOS induction.
    • An SOS-controlled inhibitor of adaptive mutation, PsiB, was discovered.

    Conclusions:

    • Adaptive mutation in Escherichia coli is a tightly regulated process controlled by the SOS system.
    • The SOS response provides both positive (e.g., RecF) and negative (e.g., PsiB) regulation of adaptive mutation.
    • This study reveals key molecular players in a stress-induced genetic variability mechanism.