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Repair and plasmid R46 mediated mutation requires inducible functions in Proteus mirabilis

Molecular & General Genetics : MGG
|January 1, 1981
PubMed

Insights

UV radiation induces Rec protein formation in Proteus mirabilis, enhancing DNA repair and mutagenesis. Plasmid R46 mediates UV mutagenesis, requiring inducible functions that are inhibited by chloramphenicol and starvation.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Proteus mirabilis exhibits inducible DNA repair and mutagenesis pathways.
  • Plasmid R46 enhances UV mutability in P. mirabilis.
  • Nalidixic acid and UV radiation can induce Rec protein formation.

Purpose of the Study:

  • To investigate the role of inducible functions in plasmid R46-mediated UV mutagenesis in P. mirabilis.
  • To determine the effect of Rec protein levels on UV mutagenesis.
  • To elucidate the mechanisms underlying UV-induced mutations.

Main Methods:

  • Induction of Rec protein formation using nalidixic acid or UV radiation.
  • Assessment of UV-induced rifampicin mutations in the presence of plasmid R46.
  • Inhibition studies using chloramphenicol and starvation.
  • Analysis of Rec protein synthesis using recombinant plasmids.

Main Results:

  • Inducible functions for post-UV replication repair and enhancement are present in P. mirabilis.
  • Plasmid R46-mediated UV mutagenesis requires additional inducible functions beyond those induced by nalidixic acid.
  • Nalidixic acid pretreatment enables efficient UV induction of mutations without post-UV incubation.
  • Chloramphenicol and starvation inhibit the inducible qualification of R46-mediated mutagenesis.
  • High-level constitutive Rec protein synthesis reduces R46-mediated UV mutagenesis.

Conclusions:

  • Plasmid R46-mediated UV mutagenesis in P. mirabilis is dependent on inducible cellular functions.
  • These inducible functions are distinct from constitutive Rec protein synthesis.
  • Understanding these mechanisms is crucial for comprehending bacterial DNA repair and mutagenesis.

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