Roles of the recJ and recQ proteins in spontaneous formation of deletion mutations in the Escherichia coli K12 endogenous tonB gene

Kazumi Mashimo, Masakado Kawata, Kazuo Yamamoto

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1 Citation (Scopus)

Abstract

The endogenous tonB gene of Escherichia coli was used as a target for spontaneous deletion mutations which were isolated from recJ- and recQ- cells. Large deletions, due to simultaneous mutations of the trp operon, were also isolated. The rates of tonB mutation were 2.77 × 10-8, 4.13 × 10-8 and 5.00 × 10-8 for rec+, recJ- and recQ- cells, respectively. We analyzed 94 and 99 tonB mutants from the recJ- and recQ- cells, respectively, by sequencing. We found that IS insertion dominated, followed by base substitutions, frameshifts and deletions in both recJ- and recQ- strains. We then analyzed 55 tonB-trp deletions, ranging in size from 5907 to 20 832 bp, from the recJ- strains and 47 tonB-trp deletions, ranging in size from 4959 to 16 390 bp from the recQ- strains. About one-third of tonB-trp deletions from both the recJ- and the recQ- cells were found to have occurred between short sequence repeats at the deletion termini. About one-third of tonB-trp deletions from both mutants showed 2-4 bp repeats in the immediate vicinity of the endpoints, which appeared to indicate no clear association with deletion. The remaining one-third of tonB-trp deletions had no homology at the endpoint. These results were similar to those for the rec+ cells. Hanada and colleagues demonstrated that structually similar rearrangements arising during λ bio phage formation (illegitimate recombination) increased in the recQ- strain. To explain this discrepancy, we interpreted as distinctive the mechanism for rearrangement during transducing phage formation which is recQ-dependent and that for deletions formed in chromosomes which is recQ-independent.

Original languageEnglish
Pages (from-to)355-363
Number of pages9
JournalMutagenesis
Volume18
Issue number4
DOIs
Publication statusPublished - 2003 Jul

ASJC Scopus subject areas

  • Genetics
  • Toxicology
  • Genetics(clinical)
  • Health, Toxicology and Mutagenesis

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