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Related Experiment Videos

Programmed cell death in bacteria: translational repression by mRNA end-pairing

T Franch1, K Gerdes

  • 1Department of Molecular Biology, Odense University, Denmark.

Molecular Microbiology
|September 1, 1996
PubMed
Summary

Plasmid maintenance systems use stable killer mRNAs (hok/pnd) and unstable antisense RNAs. Fold-back inhibition (fbi) elements sequester translational activators (tac) in inert mRNAs until 3' processing removes fbi, enabling translation.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Microbiology

Background:

  • Plasmid maintenance relies on toxic gene expression systems like hok/sok and pnd.
  • These systems utilize stable killer mRNAs and unstable antisense RNAs for regulation.
  • Previous work identified negative translational control elements in hok and pnd mRNAs.

Purpose of the Study:

  • To elucidate the regulatory mechanisms of hok and pnd mRNA translation.
  • To investigate the role of 3' fold-back inhibition (fbi) elements in mRNA regulation.
  • To identify and characterize translational activators (tac) at the 5' end of these mRNAs.

Main Methods:

  • Genetic complementation assays to study mRNA-protein interactions.
  • Mutational analyses to investigate the function of fbi and tac elements.

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  • 3' exonucleolytical processing assays to determine processing rates and effects.
  • Main Results:

    • 3' fbi elements pair with 5' mRNA ends, maintaining an inert configuration and low processing rate.
    • Translational activators (tac) at the 5' end are sequestered by fbi elements in full-length mRNAs.
    • 3' processing removes fbi elements, triggering 5' end refolding and enabling translation by unmasking tac elements.

    Conclusions:

    • The hok and pnd mRNA regulatory system involves a novel mechanism of translational control.
    • 3' processing is crucial for activating translation by removing inhibitory elements and facilitating mRNA refolding.
    • This intricate regulation ensures efficient plasmid maintenance through controlled expression of toxic genes.