The Mutagenesis Proteins UmuD' and UmuC Prevent Lethal Frameshifts While Increasing Base Substitution Mutations

Mol Cell. 1998 Aug;2(2):191-9. doi: 10.1016/s1097-2765(00)80129-x.

Abstract

Error-prone DNA repair consists of replicative filling-in of DNA gaps carrying lesions. We have reconstituted E. coli SOS error-prone repair using purified DNA polymerase III holoenzyme, SSB, RecA, UmuD', a UmuC fusion protein, and a gap lesion plasmid. In the absence of UmuDC, or without SOS induction, replication skips over the lesion, forming mostly one-nucleotide deletions. These cause translational frameshifts that usually inactivate genes. UmuD' and UmuC, in the presence of RecA and SSB, stimulate translesion replication and change its mutagenic specificity such that deletions are prevented and base substitutions are increased. This results in mutagenic but nondetrimental gap repair and provides an effective mechanism for generating genetic variation in bacteria adapting to environmental stress.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Bacterial Proteins / genetics*
  • Bacterial Proteins / metabolism
  • Base Sequence
  • DNA Primers / genetics
  • DNA Repair
  • DNA Replication
  • DNA, Bacterial / genetics
  • DNA, Bacterial / metabolism
  • DNA-Directed DNA Polymerase
  • Escherichia coli / genetics
  • Escherichia coli / metabolism
  • Escherichia coli Proteins*
  • Frameshift Mutation
  • Genes, Bacterial
  • Mutagenesis*
  • Point Mutation
  • SOS Response, Genetics

Substances

  • Bacterial Proteins
  • DNA Primers
  • DNA, Bacterial
  • Escherichia coli Proteins
  • UmuC protein, E coli
  • DNA-Directed DNA Polymerase
  • UmuD protein, E coli