Independent integration of genes controlling the invasive properties and streptomycin resistance of enteropathogenic strain Escherichia coli 0124

1976 ◽  
Vol 82 (3) ◽  
pp. 1434-1435 ◽  
Author(s):  
L. M. Aleksin ◽  
L. B. Borisov
Keyword(s):  
Escherichia Coli ◽  
Streptomycin Resistance ◽  
Enteropathogenic Strain

scholarly journals Specific phenotypic, genomic, and fitness evolutionary trajectories toward streptomycin resistance induced by pesticide co-stressors in Escherichia coli

2021 ◽  
Vol 1 (1) ◽  
Author(s):  
Yue Xing ◽  
Xiaoxi Kang ◽  
Siwei Zhang ◽  
Yujie Men
Keyword(s):  
Escherichia Coli ◽  
Antibiotic Resistance ◽  
Selective Pressure ◽  
Fold Increase ◽  
Streptomycin Resistance ◽  
Evolutionary Stage ◽  
Fitness Costs ◽  
Evolutionary Trajectories ◽  
K 12 ◽  
Late Stages

AbstractTo explore how co-occurring non-antibiotic environmental stressors affect evolutionary trajectories toward antibiotic resistance, we exposed susceptible Escherichia coli K-12 populations to environmentally relevant levels of pesticides and streptomycin for 500 generations. The coexposure substantially changed the phenotypic, genotypic, and fitness evolutionary trajectories, resulting in much stronger streptomycin resistance (>15-fold increase) of the populations. Antibiotic target modification mutations in rpsL and rsmG, which emerged and dominated at late stages of evolution, conferred the strong resistance even with less than 1% abundance, while the off-target mutations in nuoG, nuoL, glnE, and yaiW dominated at early stages only led to mild resistance (2.5–6-fold increase). Moreover, the strongly resistant mutants exhibited lower fitness costs even without the selective pressure and had lower minimal selection concentrations than the mildly resistant ones. Removal of the selective pressure did not reverse the strong resistance of coexposed populations at a later evolutionary stage. The findings suggest higher risks of the selection and propagation of strong antibiotic resistance in environments potentially impacted by antibiotics and pesticides.

scholarly journals GENETIC ANALYSIS OF STREPTOMYCIN RESISTANCE IN ESCHERICHIA COLI

Genetics ◽  
1970 ◽  
Vol 65 (1) ◽  
pp. 9-25
Author(s):  
Lee Breckenridge ◽  
Luigi Gorini
Keyword(s):  
Escherichia Coli ◽  
Genetic Analysis ◽  
Streptomycin Resistance

Characterization of the drug resistance plasmid R2418: restriction map and role of insertion and deletion in its evolution

1996 ◽  
Vol 42 (1) ◽  
pp. 12-18 ◽  
Author(s):  
Mohamed Guessouss ◽  
Kamel Ben-Mahrez ◽  
Cherifa Belhadj ◽  
Omrane Belhadj
Keyword(s):  
Escherichia Coli ◽  
Donor Cell ◽  
Streptomycin Resistance ◽  
Conjugal Transfer ◽  
Conjugative Plasmid ◽  
Restriction Map ◽  
Insertion And Deletion ◽  
Endonuclease Mapping

Escherichia coli 2418 strain is resistant to β-lactam antibiotics (ampicillin, carbenicillin, and cephalothin), streptomycin, tetracycline, kanamycin, and chloramphenicol. This strain contains at least two conjugative plasmids (R2418 and R2418S) encoding resistance to β-lactam antibiotics and resistance to both β-lactam antibiotics and streptomycin, respectively. Restriction endonuclease mapping of plasmid DNAs indicates that the plasmid R2418S has evolved from R2418 DNA by the insertion of 2.5-kb DNA between BamHI and PvuII sites, and deletion of 0.5-kb DNA within the EcoRI–EcoRV region. The 2.5-kb DNA insert is responsible for streptomycin resistance. This evolution is also associated with a reduction in the efficiency of conjugal transfer for the plasmid R2418S. The conjugal transfer of streptomycin resistance occurs only through the coresidence of the conjugative plasmid R2418 or R2418S in the donor cell. In accordance with the hypothesis that the Smr determinant is due to a putative transposon, plasmid-free transconjugants resistant to streptomycin only were isolated. Southern blot analysis of HindIII chromosomal digests extracted from these transconjugants shows that the Smr determinant is inserted into different sites in chromosomal DNA.Key words: Escherichia coli, antibiotic resistance, conjugation, transformation, plasmid, transposon, restriction map.

Enzymatic Adenylylation of Streptomycin and Spectinomycin by R-Factor-Resistant Escherichia coli

1970 ◽  
Vol 1 (1) ◽  
pp. 109-119
Author(s):  
R. Benveniste ◽  
T. Yamada ◽  
J. Davies
Keyword(s):  
Escherichia Coli ◽  
Protein Fraction ◽  
Streptomycin Resistance ◽  
Enzymatic Activities ◽  
Spectinomycin Resistance ◽  
R Factor ◽  
Temperature Inactivation ◽  
Alcohol Moiety

A resistance (R) factor- containing strain of Escherichia coli which is known to inactivate streptomycin by adenylylation has been shown to be spectinomycin resistant. An osmotic shockate of this strain catalyzes the formation of the biologically inactive spectinomycin adenylate, in which the adenylyl residue is probably attached to a d - threo methylamino alcohol moiety of spectinomycin. Both the streptomycin and spectinomycin adenylylating activities show the same temperature inactivation profile, and both are present in a protein fraction purified for the streptomycin inactivating enzyme. Mutants obtained from this strain which were sensitive to either spectinomycin or streptomycin were shown to lack both enzymatic activities when tested in vitro. Revertants of these mutants selected for recovery of either streptomycin resistance or spectinomycin resistance regain both activities. Therefore, we conclude that the inactivation of the two drugs is catalyzed by the same enzyme. Examination of a number of R factor-carrying strains has shown that those strains which are resistant to streptomycin and spectinomycin contain the adenylylating enzyme, whereas strains resistant to streptomycin but sensitive to spectinomycin inactivate streptomycin by phosphorylation.

scholarly journals COLONIZATION OF THE MOUSE INTESTINE WITH ESCHERICHIA COLI

1965 ◽  
Vol 122 (4) ◽  
pp. 745-757 ◽  
Author(s):  
Rose Mushin ◽  
Rene Dubos
Keyword(s):  
Escherichia Coli ◽  
Gastrointestinal Tract ◽  
Intestinal Tract ◽  
Intestinal Infection ◽  
Stomach Tube ◽  
E Coli ◽  
Swiss Mice ◽  
Suggestive Evidence ◽  
Enteropathogenic Strain ◽  
Mouse Intestine

Young albino Swiss mice, of the NCS and NCS-D colonies, proved highly susceptible to the establishment of intestinal infection with an enteropathogenic strain of E. coli administered per os or by stomach tube. The period of highest susceptibility was rather short, extending from the day of birth to approximately 2 weeks of age. Adult NCS and NCS-D mice failed to become experimentally colonized with E. coli, even when large doses were administered per os on 3 consecutive days. The extent of colonization of the various parts of the gastrointestinal tract was related to the size of the infective dose. Many of the young mice died within 2 to 3 days following per os infection with large doses of enteropathogenic E. coli. However, practically all the animals which survived cleared their intestinal infection at approximately the same age. For example, in mice infected with 23 x 106 bacteria, colonization of the intestinal tract usually came to an abrupt end when the animals were 24 to 28 days old, irrespective of the age at which they had been infected. There is suggestive evidence that the acquisition of resistance with age, and the ability of adult animals to control the intestinal infection, are related to the development in the gastrointestinal tract of a microbiota which is antagonistic to E. coli.

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