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Related Experiment Videos

Tn10 transposition promotes RecA-dependent induction of a lambda prophage.

D Roberts1, N Kleckner

  • 1Department of Biochemistry and Molecular Biology, Harvard University, Cambridge, MA 02138.

Proceedings of the National Academy of Sciences of the United States of America
|August 1, 1988
PubMed
Summary

Transposon Tn10 triggers bacterial SOS responses, including lambda prophage induction and sfiA gene expression in E. coli. This likely aids cell recovery from DNA damage during transposition.

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Area of Science:

  • Molecular Biology
  • Bacterial Genetics
  • DNA Transposition

Background:

  • Bacterial SOS functions are DNA damage-inducible stress responses.
  • Transposable elements like Tn10 can influence host cell processes.
  • The RecA protein is central to SOS response activation.

Purpose of the Study:

  • To investigate if Tn10 transposition induces bacterial SOS functions.
  • To elucidate the mechanism by which Tn10 might trigger SOS.
  • To understand the biological significance of SOS induction during transposition.

Main Methods:

  • Assessed lambda prophage induction in Escherichia coli lysogens with varying Tn10 transposase levels and transposon ends.
  • Measured induction of the E. coli sfiA gene.

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  • Utilized knowledge of RecA-mediated cleavage of phage lambda repressor.

    • Main Results:

    • Increased Tn10 transposase function and transposon ends elevated lambda prophage induction via RecA.
    • Tn10 was shown to promote the induction of E. coli sfiA gene expression.
    • Tn10 transposition occurs via a nonreplicative mechanism.

    Conclusions:

    • Tn10 transposition, or a related event, directly induces bacterial SOS functions.
    • Degradation of the transposon donor molecule may generate the signal for RecA protease activation.
    • SOS induction likely facilitates cellular repair and recovery from DNA damage during Tn10 transposition.