scholarly journals Resistance ofEscherichia colito penicillins: III. AmpB, a locus affecting episomally and chromosomally mediated resistance to ampicillin and chloramphenicol

1968 ◽  
Vol 12 (2) ◽  
pp. 157-168 ◽  
Author(s):  
Kurt Nordström ◽  
Kerstin G. Eriksson-Grennberg ◽  
Hans G. Boman
Keyword(s):  
Escherichia Coli ◽  
Additive Effects ◽  
Wild Type ◽  
Chloramphenicol Resistance ◽  
Ampicillin Resistance ◽  
Modifying Genes ◽  
R Factor ◽  
Chromosomal Genes ◽  
R Factors

We have previously described strains ofEscherichia coliK12 resistant to D, L-ampicillin concentrations of 50 μg/ml (Eriksson-Grennberget al.1965; Bomanet al.1967). Such strains were assumed to be double mutants carrying the genesampAandampB. We here describe genetic steps which produce strains carrying only theampBgene. Determinations of resistance showed thatampAincreased the resistance provided byampA+by a factor of 10–15.AmpBincreased the resistance of bothampAandampA+by a factor of 2.R-factors were introduced into two sets of strains with all combinations ofampA,ampBand their wild type alleles.AmpAand the R-factors gave additive effects on resistance, whileampBdoubled the ampicillin resistance mediated byampAas well as by the R-factors.AmpBalso enhanced the chloramphenicol resistance of R-factor and of the wild type chromosomal genes. It is suggested thatampBresembles the modifying genes previously described and that R-factors can be useful for the identification of such genes.

scholarly journals Recombination and complementation between R factors inEscherichia coliK 12

1971 ◽  
Vol 18 (3) ◽  
pp. 287-297 ◽  
Author(s):  
T. J. Foster ◽  
T. G. B. Howe
Keyword(s):  
Escherichia Coli ◽  
Specific Activity ◽  
Chloramphenicol Acetyl Transferase ◽  
Wild Type ◽  
Chloramphenicol Resistance ◽  
Low Level ◽  
R Factor ◽  
Reduced Frequency ◽  
Interallelic Complementation ◽  
R Factors

SUMMARYRecombination between chloramphenicol-sensitive (Cms) mutants of Rl, and R100, has been demonstrated inEscherichia coliK12rec+; it occurs at reduced frequency inrecBandrecC, and is not detectable inreeA, indicating that R factor recombination depends on host functions. Some mutants of R1 also recombine with an R100 mutant in a similar way.recAcells carrying an R1 and an R100 Cmsmutant (hetero-R state) have a low level of chloramphenicol-resistance, and form a chloramphenicol acetyl transferase that has lower specific activity than enzyme from hosts carrying wild-type or recombinant factors. These results suggest the occurrence of interallelic complementation between mutant R factors.

scholarly journals Characteristics of some single-step mutants to chloramphenicol resistance in Escherichia coli K12 and their interactions with R-factor genes

1966 ◽  
Vol 7 (2) ◽  
pp. 281-286 ◽  
Author(s):  
E. C. R. Reeve
Keyword(s):  
Escherichia Coli ◽  
Single Step ◽  
Chloramphenicol Resistance ◽  
R Factor ◽  
Resistance Patterns ◽  
One Step ◽  
Increased Sensitivity ◽  
Resistant Mutants ◽  
High Level ◽  
R Factors

Six one-step Chloramphenicol (Cm)-resistant mutants of Escherichia coli K12 were graded for resistance to Cm, Tetracycline (Tc) and Puromyein (Pm) by streaking on minimal agar plates containing antibiotic. They fell into at least three distinct groups on the basis of their resistance patterns. One mutant showed increased sensitivity to Pm. Most of the mutants expressed their effect on resistance to Cm and Tc in the presence of R-factors carrying resistance genes for these antibiotics, but one mutant with a relatively high level of resistance to Cm had its resistance effect completely masked in the presence of R-mediated resistance. Similar cases were found among mutants selected for Cm-resistance in another strain of K12.

scholarly journals The characteristics of eleven mutants of R-factor R57 constitutive for tetracycline resistance, selected and tested inEscherichia coliK12

1975 ◽  
Vol 25 (3) ◽  
pp. 297-311 ◽  
Author(s):  
E. C. R. Reeve ◽  
J. M. Robertson
Keyword(s):  
Escherichia Coli ◽  
Constitutive Expression ◽  
Tetracycline Resistance ◽  
Gene Products ◽  
Wild Type ◽  
Repressor Gene ◽  
Negative Type ◽  
R Factor

SUMMARYEleven mutants of R-factor R57 have been isolated which show constitutive expression of resistance to tetracycline (Tc). These derepressed (Tdr) mutants all gave a much greater resistance to Tc and to its analogue, minocycline, than could be obtained by optimal induction of cells carrying the wild-type (T+) determinant. Cells carrying each of the Tdr mutants together with T+of either R6-S or of a plasmid found inEscherichia colimi19 showed inducible Tc resistance, indicating that the Tdr mutants were all recessive, i.e. of repressor-negative type. Tdr1 was not recessive to the T-determinant of RP1, suggesting that the repressor gene products of the T-determinants in R57 and RP1 have different specificities.

scholarly journals Characterization and nucleotide sequence of the cryptic cel operon of Escherichia coli K12.

Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 455-471 ◽  
Author(s):  
L L Parker ◽  
B G Hall
Keyword(s):  
Escherichia Coli ◽  
Nucleotide Sequence ◽  
Regulatory Protein ◽  
Wild Type ◽  
Phosphotransferase System ◽  
E Coli ◽  
Significant Homology ◽  
Chromosomal Genes ◽  
Alpha Galactosidase ◽  
Beta Glucosidase

Abstract Wild-type Escherichia coli are not able to utilize beta-glucoside sugars because the genes for utilization of these sugars are cryptic. Spontaneous mutations in the cel operon allow its expression and enable the organism to ferment cellobiose, arbutin and salicin. In this report we describe the structure and nucleotide sequence of the cel operon. The cel operon consists of five genes: celA, whose function is unknown; celB and celC which encode phosphoenolpyruvate-dependent phosphotransferase system enzyme IIcel and enzyme IIIcel, respectively, for the transport and phosphorylation of beta-glucoside sugars; celD, which encodes a negative regulatory protein; and celF, which encodes a phospho-beta-glucosidase that acts on phosphorylated cellobiose, arbutin and salicin. The mutationally activated cel operon is induced in the presence of its substrates, and is repressed in their absence. A comparison of proteins encoded by the cel operon with functionally equivalent proteins of the bgl operon, another cryptic E. coli gene system responsible for the catabolism of beta-glucoside sugars, revealed no significant homology between these two systems despite common functional characteristics. The celD and celF encoded repressor and phospho-beta-glucosidase proteins are homologous to the melibiose regulatory protein and to the melA encoded alpha-galactosidase of E. coli, respectively. Furthermore, the celC encoded PEP-dependent phosphotransferase system enzyme IIIcel is strikingly homologous to an enzyme IIIlac of the Gram-positive organism Staphylococcus aureus. We conclude that the genes for these two enzyme IIIs diverged much more recently than did their hosts, indicating that E. coli and S. aureus have undergone relatively recent exchange of chromosomal genes.

scholarly journals Properties of the R factor R144drd3 inKlebsiella pneumoniaestrain M5a1

1975 ◽  
Vol 25 (3) ◽  
pp. 327-338 ◽  
Author(s):  
R. Dixon ◽  
F. C. Cannon ◽  
J. R. Postgate
Keyword(s):  
Escherichia Coli ◽  
Drug Resistance ◽  
Klebsiella Pneumoniae ◽  
Donor Strain ◽  
R Factor ◽  
Chromosomal Genes ◽  
Successive Subculture ◽  
Autonomous State

SUMMARYThe R factor, R144drd3, mobilized chromosomal genes inKlebsiella pneumoniaestrain M5a1 at similar frequencies to those observed for this R factor inEscherichia coliK12. In a derivativeK. pneumoniaedonor, strain HF3, R144 persisted in the autonomous state but now gave rise to polarized transfer of the chromosome in the order Ohis…arg2…leu…trp. R144drd3 was unstable inK. pneumoniaeM5a1; after successive subculture drug resistance, colicinogeny and transmissibility were lost. In strain HF3, transmissibility was preferentially lost, but determinants for drug resistance, colicinogeny and superinfection immunity were retained; 10–11 copies per chromosome of R144 were present in log phase cultures of both strains.

scholarly journals Change of host range in a resistance factor

1970 ◽  
Vol 16 (2) ◽  
pp. 207-214 ◽  
Author(s):  
E. S. Anderson ◽  
E. J. Threlfall
Keyword(s):  
Escherichia Coli ◽  
Host Range ◽  
Host Specificity ◽  
Salmonella Enteritidis ◽  
Streptomycin Resistance ◽  
Resistance Factor ◽  
R Factor ◽  
R Factors

SUMMARYAn R factor for ampicillin and streptomycin resistance (AS) was identified inSalmonella enteritidis. The AS factor transferred freely toEscherichia coliK12, but only two of 260 K12(AS) clones from this cross would transfer AS toS. typhimurium, although all lines tested transferred it toS. enteritidisand K12. A study of one of the two exceptional lines“ revealed that it also transferred AS toS. paratyphiB,S. thompsonandS. anatum. The R factor maintained its transferability when cycled between these serotypes and K12. Transfer toS. enteritidis, however, resulted in loss of the ability of AS to transfer to the heterologous serotypes, that is, it apparently became host specific forS. enteritidis. S. paratyphiB andS. anatumalso imposed host specificity on AS, butS. typhimuriumandS. thompsondid not. The R factor would always enterS. enteritidis, whatever its previous salmonella host but, once it had done so, it became specific forS. enteritidis. AS could always transfer to K12, which did not seem to modify its host range. These phenomena are most easily explained by analogy with host-controlled modification of phage. Their possible significance in relation to apparent host specificity of R factors is discussed.

scholarly journals Trimethoprim-resistance and its transferability in E. coli isolated from calves treated with trimethoprim-sulphadiazine: a two year study

1973 ◽  
Vol 71 (4) ◽  
pp. 669-677 ◽  
Author(s):  
M. P. Fleming
Keyword(s):  
Escherichia Coli ◽  
Enteric Bacteria ◽  
Streptomycin Resistance ◽  
Serological Evidence ◽  
E Coli ◽  
R Factor ◽  
Oral Doses ◽  
R Factors ◽  
Higher Doses

SummaryRegular examination of rectal swabs revealed the presence of very low numbers of trimethoprim resistant Escherichia coli in the faeces of 10 batches of calves successively reared in the same shed and none of these strains transferred trimethoprim resistance to E. coli K12. All the calves had received oral doses of 30 mg/kg day of trimethoprim-sulphadiazine for 5 consecutive days. From two subsequent batches of calves reared in the same shed, however, several isolations were made of E. coli with transmissible R factors determining trimethoprim and streptomycin resistance. Shortly before these strains were detected, isolations of E. coli with similar properties had been made from other calves, in a different shed, which had been fed much higher doses of trimethoprim-sulphadiazine. Serological evidence indicated that all the E. coli isolated carrying this R factor belonged to the same strain, which had apparently spread from the second shed to the first. No evidence of ‘in vivo’ transfer of the R factor to other enteric bacteria was obtained.

scholarly journals Functional Analysis ofycfRandycfQin Escherichia coli O157:H7 Linked to Outbreaks of Illness Associated with Fresh Produce

2011 ◽  
Vol 77 (12) ◽  
pp. 3952-3959 ◽  
Author(s):  
Kaiping Deng ◽  
Siyun Wang ◽  
Xiaoqian Rui ◽  
Wei Zhang ◽  
Mary Lou Tortorello
Keyword(s):  
Escherichia Coli ◽  
Fresh Produce ◽  
The United States ◽  
Sublethal Concentration ◽  
Wild Type ◽  
Chloramphenicol Resistance ◽  
Content Type ◽  
E Coli ◽  
K 12 ◽  
Postharvest Processing

ABSTRACTFresh produce has been associated with multiple outbreaks of illness caused byEscherichia coliO157:H7. The mechanism ofE. coliO157:H7 survival through postharvest processing of fresh produce needs to be understood to help develop more effective interventions. In our recent transcriptomic study of strain Sakai, an isolate from the 1996 sprout outbreak in Japan, and strain TW14359, an isolate from the 2006 spinach outbreak in the United States, we showed thatycfRwas the most significantly upregulated gene in response to chlorine-based oxidative stress. YcfR is known to be a multiple stress resistance protein and a biofilm regulator inE. coliK-12 strains; however, its role in the pathogenicE. coliO157:H7 has not been clearly defined. In this study,ycfRwas replaced with a chloramphenicol resistance cassette oriented in two different directions to construct polar and nonpolarycfR::catmutants of Sakai and TW14359. Chlorine resistance and survival on spinach leaf surfaces were assessed in the wild-type strains and theycfRmutants. Both polar and nonpolarycfRmutants of Sakai showed significantly less chlorine resistance than their parent strain. In contrast, deletion ofycfRin TW14359 did not change chlorine resistance, indicating thatycfRin these two outbreak-relatedE. coliO157:H7 strains may function differently. In addition, after a 24-h incubation on spinach leaves in a sublethal concentration of chlorine, the Sakai nonpolarycfRmutant exhibited lower survival compared to the wild type. The results suggest a role forycfRin survival of Sakai during chlorine exposure. We also found that the upstreamycfQ, which is annotated as a DNA-binding regulator, acted as a repressor ofycfR. These findings suggest that gene regulation may be a mechanism by whichE. coliO157:H7 strain Sakai could survive in the postharvest processing environment.

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