TY - JOUR
T1 - Role of the RuvAB protein in avoiding spontaneous formation of deletion mutations in the Escherichia coli K-12 endogenous tonB gene
AU - Mashimo, Kazumi
AU - Nagata, Yuki
AU - Kawata, Masakado
AU - Iwasaki, Hiroshi
AU - Yamamoto, Kazuo
N1 - Funding Information:
This work was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan.
PY - 2004/10/8
Y1 - 2004/10/8
N2 - The endogenous tonB gene of Escherichia coli was used as a target for spontaneous deletion mutations which were isolated from ruvAB -, recG -, and ruvC - cells. The rates of tonB mutation were essentially the same in ruv +, ruvAB -, recG -, and ruvC - cells. We analyzed tonB mutants by sequencing. In the ruv +, recG -, and ruvC - strains, the spectra were different from those obtained from the ruvAB - cells, where deletions dominated followed by IS insertions, base substitutions, and frameshifts, in that order. We then analyzed the tonB-trp large deletion, due to simultaneous mutations of the trp operon, and found that the frequency in ruvAB - was higher than those in ruv +, recG -, and ruvC - cells. To characterize deletion formation further, we analyzed all the tonB mutants from one colicin plate. Seven deletions were identified at five sites from the 45 tonB mutants of ruv + cells and 24 deletions at 11 sites from the 43 tonB mutants of ruvAB - cells. Thus, the ruvAB - strain is a deletion mutator. We discuss the role of RuvAB in avoiding deletions.
AB - The endogenous tonB gene of Escherichia coli was used as a target for spontaneous deletion mutations which were isolated from ruvAB -, recG -, and ruvC - cells. The rates of tonB mutation were essentially the same in ruv +, ruvAB -, recG -, and ruvC - cells. We analyzed tonB mutants by sequencing. In the ruv +, recG -, and ruvC - strains, the spectra were different from those obtained from the ruvAB - cells, where deletions dominated followed by IS insertions, base substitutions, and frameshifts, in that order. We then analyzed the tonB-trp large deletion, due to simultaneous mutations of the trp operon, and found that the frequency in ruvAB - was higher than those in ruv +, recG -, and ruvC - cells. To characterize deletion formation further, we analyzed all the tonB mutants from one colicin plate. Seven deletions were identified at five sites from the 45 tonB mutants of ruv + cells and 24 deletions at 11 sites from the 43 tonB mutants of ruvAB - cells. Thus, the ruvAB - strain is a deletion mutator. We discuss the role of RuvAB in avoiding deletions.
KW - Deletion
KW - Replication fork collapse
KW - Spontaneous mutagenesis
KW - recG
KW - ruvAB
KW - ruvC
KW - tonB gene
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U2 - 10.1016/j.bbrc.2004.08.078
DO - 10.1016/j.bbrc.2004.08.078
M3 - Article
C2 - 15351721
AN - SCOPUS:4444328986
SN - 0006-291X
VL - 323
SP - 197
EP - 203
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -