scholarly journals DELETIONS GENERATED BY THE TRANSPOSON Tn10 IN THE srl recA REGION OF THE ESCHERICHIA COLI K-12 CHROMOSOME

Genetics ◽  
1979 ◽  
Vol 93 (2) ◽  
pp. 321-343
Author(s):  
LÁszlÓ N Csonka ◽  
Alvin J Clark

ABSTRACT A negative regulatory gene for the srl operon (srlR) was recognized by the characteristics of an insertion mutation generated by the transposon TnlO determining tetracycline resistance. This finding is discussed in light of previous hypotheses on the regulation of the srl genes, which mediate metabolism of glucitol (i.e, sorbitol). Mapping showed that the order of genes in this region is: srlR srlD srlC recA alaS. Using two different methods, five mutations of both srl and recA were detected. The phenotype conferred by these mutations, UV sensitivity and extreme recombination deficiency, is characteristic of standard recA point mutants. Three of the mutations were deletions that also removed the genes for tetracycline resistance of the nearby transposon. A fourth mutation ended at a distance from Tn10 sufficient to allow separation of the two by recombination following P1 transduction; our tests did not allow US to conclude whether this mutation was an inversion or a deletion. The fifth mutation was a deletion that seemed to end immediately adjacent to the boundary of Tn10. proximal to recA. Mechanisms for the generaticn of these srl recA mutations are discussed.

1994 ◽  
Vol 13 (1) ◽  
pp. 35-49 ◽  
Author(s):  
Ho-Ching Tiffany Tsui ◽  
Hon-Chiu Eastwood Leung ◽  
Malcolm E. Winkler

2007 ◽  
Vol 190 (4) ◽  
pp. 1491-1494 ◽  
Author(s):  
Ricardo E. de Cristóbal ◽  
Paula A. Vincent ◽  
Raúl A. Salomón

ABSTRACT Previously, we demonstrated that Escherichia coli tolC mutations reduce the high-level resistance to tetracycline afforded by the transposon Tn10-encoded TetA pump from resistance at 200 μg/ml to resistance at 40 μg/ml. In this study, we found that the addition of an sbmA mutation to a tolC::Tn10 mutant exacerbates this phenotype: the double mutant did not form colonies, even in the presence of tetracycline at a concentration as low as 5 μg/ml. Inactivation of sbmA alone partially inhibited high-level tetracycline resistance, from resistance at 200 μg/ml to resistance at 120 μg/ml. There thus appears to be an additive effect of the mutations, resulting in almost complete suppression of the phenotypic expression of Tn10 tetracycline resistance.


1981 ◽  
Vol 27 (6) ◽  
pp. 616-626 ◽  
Author(s):  
M. Konarska-Kozlowska ◽  
V. N. Iyer

The nature and basis of variability in the conjugational behaviour of RM98+ (RM98-carrying) strains of Escherichia coli K-12 that are otherwise similar in phenotype was studied. An explanation for such variability is provided.Some RM98+ strains of E. coli have a plasmid aggregate, which upon conjugation yields two different conjugative plasmids. The first (pCU1) is an N conjugative group plasmid by all available criteria. The second (pCU2) could not be placed in any conjugative group known among the Enterobacteriaceae. Reciprocal DNA hybridization experiments and the gel patterns displayed by the two plasmid DNAs upon digestion with different restriction endonucleases indicate no extensive sequence homology between pCU1 and pCU2. pCU2 DNA is much longer than pCU1 DNA.Despite the absence of extensive homology, the DNA of pCU1 and pCU2 can interact. Derivatives can be selected that have all the antibiotic markers of the aggregate plasmid but that neither contain nor segregate pCU2. It is shown that in such strains a DNA fragment of molecular weight 7.9 × 106 has been added to pCU1 concurrently with a tetracycline resistance marker originally present in pCU2 and absent in pCU1. These observations suggest that tetracycline resistance in pCU2 may be part of a large translocatable element.RM98 has been used to designate a reference Inc N group plasmid. The results presented indicate that this can lead to ambiguity. pCU1 would now be the appropriate reference plasmid.


2001 ◽  
Vol 45 (5) ◽  
pp. 1467-1472 ◽  
Author(s):  
A. S. Jellen-Ritter ◽  
W. V. Kern

ABSTRACT The development of fluoroquinolone resistance in Escherichia coli may be associated with mutations in regulatory gene loci such as marRAB that lead to increased multidrug efflux, presumably through activation of expression of the AcrAB multidrug efflux pump. We found that multidrug-resistant (MDR) phenotypes with enhanced efflux can also be selected by fluoroquinolones frommarRAB- or acrAB-inactivated E. coli K-12 strains having a single mutation in the quinolone-resistance-determining region of gyrA. Mutant 3-AG100MKX, obtained from a mar knockout strain after two selection steps, showed enhanced expression of acrB in a reverse transcriptase PCR associated with insertion of IS186 into the AcrAB repressor gene acrR. In vitro selection experiments with acrAB knockout strains yielded MDR mutants after a single step. Enhanced efflux in these mutants was due to increased expression of acrEF and associated with insertion of IS2 into the upstream region ofacrEF, presumably creating a hybrid promoter. These observations confirm the importance of efflux-associated nontarget gene mutations and indicate that transposition of genetic elements may have a role in the development of fluoroquinolone resistance in E. coli.


1983 ◽  
Vol 189 (2) ◽  
pp. 351-354 ◽  
Author(s):  
Paul Ritzenthaler ◽  
Mireille Mata-Gilsinger

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