The response of a cytokinin resistant mutant is highly specific and permits a new cytokinin bioassay

1995 ◽  
Vol 17 (2) ◽  
pp. 87-94 ◽  
Author(s):  
F. Nogu� ◽  
M. Jullien ◽  
R. Mornet ◽  
M. Laloue
Keyword(s):  
Resistant Mutant ◽  
Cytokinin Bioassay

Comparative Proteomic and Transcriptome Analysis of Nitron-Oligomycin Resistant Mutant Streptomyces fradiae-nitR+bld Strain

2020 ◽  
Vol 56 (9) ◽  
pp. 1151-1154
Author(s):  
O. B. Bekker ◽  
A. A. Vatlin ◽  
D. A. Mavletova ◽  
L. N. Lysenkova ◽  
A. E. Shchekotikhin ◽  
...  
Keyword(s):  
Transcriptome Analysis ◽  
Resistant Mutant ◽  
Streptomyces Fradiae

scholarly journals Moxifloxacin Activates the SOS Response in Mycobacterium tuberculosis in a Dose- and Time-Dependent Manner

2021 ◽  
Vol 9 (2) ◽  
pp. 255
Author(s):  
Angelo Iacobino ◽  
Giovanni Piccaro ◽  
Manuela Pardini ◽  
Lanfranco Fattorini ◽  
Federico Giannoni
Keyword(s):  
Gene Expression ◽  
Mycobacterium Tuberculosis ◽  
Physiological State ◽  
Transcriptional Response ◽  
Sos Response ◽  
Resistant Mutant ◽  
Time Dependent ◽  
Dependent Manner ◽  
Gyra Gene ◽  
Drug Concentrations

Previous studies on Escherichia coli demonstrated that sub-minimum inhibitory concentration (MIC) of fluoroquinolones induced the SOS response, increasing drug tolerance. We characterized the transcriptional response to moxifloxacin in Mycobacterium tuberculosis. Reference strain H37Rv was treated with moxifloxacin and gene expression studied by qRT-PCR. Five SOS regulon genes, recA, lexA, dnaE2, Rv3074 and Rv3776, were induced in a dose- and time-dependent manner. A range of moxifloxacin concentrations induced recA, with a peak observed at 2 × MIC (0.25 μg/mL) after 16 h. Another seven SOS responses and three DNA repair genes were significantly induced by moxifloxacin. Induction of recA by moxifloxacin was higher in log-phase than in early- and stationary-phase cells, and absent in dormant bacilli. Furthermore, in an H37Rv fluoroquinolone-resistant mutant carrying the D94G mutation in the gyrA gene, the SOS response was induced at drug concentrations higher than the mutant MIC value. The 2 × MIC of moxifloxacin determined no significant changes in gene expression in a panel of 32 genes, except for up-regulation of the relK toxin and of Rv3290c and Rv2517c, two persistence-related genes. Overall, our data show that activation of the SOS response by moxifloxacin, a likely link to increased mutation rate and persister formation, is time, dose, physiological state and, possibly, MIC dependent.

scholarly journals Bacterial Resistance to Antisense Peptide Phosphorodiamidate Morpholino Oligomers

2012 ◽  
Vol 56 (12) ◽  
pp. 6147-6153 ◽  
Author(s):  
Susan E. Puckett ◽  
Kaleb A. Reese ◽  
Georgi M. Mitev ◽  
Valerie Mullen ◽  
Rudd C. Johnson ◽  
...  
Keyword(s):  
Bacterial Resistance ◽  
Acyl Carrier Protein ◽  
Essential Gene ◽  
Resistant Mutant ◽  
Resistant Isolate ◽  
Carrier Protein ◽  
Bacterial Gene ◽  
Content Type ◽  
Bacterial Gene Expression ◽  
Phosphorodiamidate Morpholino Oligomers

ABSTRACTPeptide phosphorodiamidate morpholino oligomers (PPMOs) are synthetic DNA mimics that bind cRNA and inhibit bacterial gene expression. The PPMO (RFF)3RXB-AcpP (where R is arginine, F, phenylalanine, X is 6-aminohexanoic acid, B is β-alanine, and AcpP is acyl carrier protein) is complementary to 11 bases of the essential geneacpP(which encodes acyl carrier protein). The MIC of (RFF)3RXB-AcpP was 2.5 μM (14 μg/ml) inEscherichia coliW3110. The rate of spontaneous resistance ofE. colito (RFF)3RXB-AcpP was 4 × 10−7mutations/cell division. A spontaneous (RFF)3RXB-AcpP-resistant mutant (PR200.1) was isolated. The MIC of (RFF)3RXB-AcpP was 40 μM (224 μg/ml) for PR200.1. The MICs of standard antibiotics for PR200.1 and W3110 were identical. The sequence ofacpPwas identical in PR200.1 and W3110. PR200.1 was also resistant to other PPMOs conjugated to (RFF)3RXB or peptides with a similar composition or pattern of cationic and nonpolar residues. Genomic sequencing of PR200.1 identified a mutation insbmA, which encodes an active transport protein. In separate experiments, a (RFF)3RXB-AcpP-resistant isolate (RR3) was selected from a transposome library, and the insertion was mapped tosbmA. Genetic complementation of PR200.1 or RR3 withsbmArestored susceptibility to (RFF)3RXB-AcpP. Deletion ofsbmAcaused resistance to (RFF)3RXB-AcpP. We conclude that resistance to (RFF)3RXB-AcpP was linked to the peptide and not the phosphorodiamidate morpholino oligomer, dependent on the composition or repeating pattern of amino acids, and caused by mutations insbmA. The data further suggest that (RFF)3R-XB PPMOs may be transported across the plasma membrane by SbmA.

scholarly journals CHROMOSOMAL BASIS OF THE MEROZYGOSITY IN A PARTIALLY DIPLOID MUTANT OF PNEUMOCOCCUS

Genetics ◽  
1975 ◽  
Vol 80 (4) ◽  
pp. 667-678
Author(s):  
Mary Lee S Ledbetter ◽  
Rollin D Hotchkiss
Keyword(s):  
High Efficiency ◽  
Point Mutations ◽  
Resistant Mutant ◽  
Chromosomal Marker ◽  
Structural Abnormality ◽  
C Cells ◽  
Wild Type ◽  
Chromosomal Locus ◽  
Low Efficiency ◽  
Derivatives Of

ABSTRACT A sulfonamide-resistant mutant of pneumococcus, sulr-c, displays a genetic instability, regularly segregating to wild type. DNA extracts of derivatives of the strain possess transforming activities for both the mutant and wild-type alleles, establishing that the strain is a partial diploid. The linkage of sulr-c to strr-61, a stable chromosomal marker, was established, thus defining a chromosomal locus for sulr-c. DNA isolated from sulr-c cells transforms two mutant recipient strains at the same low efficiency as it does a wild-type recipient, although the mutant property of these strains makes them capable of integrating classical "low-efficiency" donor markers equally as efficiently as "high efficiency" markers. Hence sulr-c must have a different basis for its low efficiency than do classical low efficiency point mutations. We suggest that the DNA in the region of the sulr-c mutation has a structural abnormality which leads both to its frequent segregation during growth and its difficulty in efficiently mediating genetic transformation.

scholarly journals In VitroAntibacterial Activity of NB-003 against Propionibacterium acnes

2011 ◽  
Vol 55 (9) ◽  
pp. 4211-4217 ◽  
Author(s):  
J. Pannu ◽  
A. McCarthy ◽  
A. Martin ◽  
T. Hamouda ◽  
S. Ciotti ◽  
...  
Keyword(s):  
Bacterial Infections ◽  
Propionibacterium Acnes ◽  
Resistant Mutant ◽  
Microtiter Plate ◽  
Content Type ◽  
Oil In Water ◽  
Complete Disruption ◽  
Kinetics Of ◽  
Gel Formulations

ABSTRACTNB-003 and NB-003 gel formulations are oil-in-water nanoemulsions designed for use in bacterial infections.In vitrosusceptibility ofPropionibacterium acnesto NB-003 formulations and comparator drugs was evaluated. Both NB-003 formulations were bactericidal against allP. acnesisolates, including those that were erythromycin, clindamycin, and/or tetracycline resistant. In the absence of sebum, the MIC90s/minimum bactericidal concentrations (MBC90s) for NB-003, NB-003 gel, salicylic acid (SA), and benzoyl peroxide (BPO) were 0.5/2.0, 1.0/2.0, 1,000/2,000, and 50/200 μg/ml, respectively. In the presence of 50% sebum, the MIC90s/MBC90s of NB003 and BPOs increased to 128/1,024 and 400/1,600 μg/ml, respectively. The MIC90s/MBC90s of SA were not significantly impacted by the presence of sebum. A reduction in the MBC90s for NB-003 and BPO was observed when 2% SA or 0.5% BPO was integrated into the formulation, resulting in MIC90s/MBC90s of 128/256 μg/ml for NB003 and 214/428 μg/ml for BPO. The addition of EDTA enhanced thein vitroefficacy of 0.5% NB-003 in the presence or absence of 25% sebum. The addition of 5 mM EDTA to each well of the microtiter plate resulted in a >16- and >256-fold decrease in MIC90and MBC90, yielding a more potent MIC90/MBC90of ≤1/<1 μg/ml. The kinetics of bactericidal activity of NB-003 againstP. acneswere compared to those of a commercially available product of BPO. Electron micrographs ofP. acnestreated with NB-003 showed complete disruption of bacteria. Assessment of spontaneous resistance ofP. acnesrevealed no stably resistant mutant strains.

scholarly journals Changes in genetic constitution and sterol composition during growth of nystatin-resistant heterokaryons ofNeurospora crassa

1983 ◽  
Vol 42 (1) ◽  
pp. 91-103 ◽  
Author(s):  
Jill E. Ogden ◽  
Morris Grindle
Keyword(s):  
Growth Rates ◽  
Minimal Medium ◽  
Resistant Mutant ◽  
Sterol Composition ◽  
Sensitive Strain ◽  
Genetic Constitution ◽  
Polyene Antibiotic ◽  
Ofneurospora Crassa ◽  
Synthetic Media ◽  
Selection Of

SUMMARYHeterokaryons ofN. crassawere synthesized from homokaryotic strains differing in sterol composition and sensitivity to the polyene antibiotic nystatin. Mycelia of the nystatin-sensitive strainerg-1+contained ergosterol and episterol, and the nystatin-resistant mutanterg-1 contained fecosterol and lichesterol. Mycelia of heterokaryons with different proportions oferg-1+:erg-1 nuclei contained various proportions of the four sterols. Ergosterol was the principal sterol in heterokaryons with more than 5%erg-1+nuclei.Heterokaryons with various proportions oferg-1+:erg-1 nuclei were grown for several weeks along tubes of synthetic media. Growth rates were stable on minimal medium and nutritionally supplemented media but nuclear proportions often fluctuated. Growth rates fell sharply on nystatin-supplemented media and there were adaptive increases in proportions of mutanterg-1 nuclei which resulted in selection of nystatin-resistant homokaryotic mycelia.

scholarly journals Activity of Ceftazidime-Avibactam against Fluoroquinolone-Resistant Enterobacteriaceae and Pseudomonas aeruginosa

2015 ◽  
Vol 59 (6) ◽  
pp. 3059-3065 ◽  
Author(s):  
C. Pitart ◽  
F. Marco ◽  
T. A. Keating ◽  
W. W. Nichols ◽  
J. Vila
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Resistant Mutant ◽  
Fluoroquinolone Resistance ◽  
Cross Resistance ◽  
Content Type ◽  
E Coli ◽  
Microdilution Method ◽  
Broth Microdilution Method ◽  
The Impact

ABSTRACTCeftazidime-avibactam and comparator antibiotics were tested by the broth microdilution method against 200Enterobacteriaceaeand 25Pseudomonas aeruginosastrains resistant to fluoroquinolones (including strains with the extended-spectrum β-lactamase [ESBL] phenotype and ceftazidime-resistant strains) collected from our institution. The MICs and mechanisms of resistance to fluoroquinolone were also studied. Ninety-nine percent of fluoroquinolone-resistantEnterobacteriaceaestrains were inhibited at a ceftazidime-avibactam MIC of ≤4 mg/liter (using the susceptible CLSI breakpoint for ceftazidime alone as a reference). Ceftazidime-avibactam was very active against ESBLEscherichia coli(MIC90of 0.25 mg/liter), ESBLKlebsiella pneumoniae(MIC90of 0.5 mg/liter), ceftazidime-resistant AmpC-producing species (MIC90of 1 mg/liter), non-ESBLE. coli(MIC90of ≤0.125 mg/liter), non-ESBLK. pneumoniae(MIC90of 0.25 mg/liter), and ceftazidime-nonresistant AmpC-producing species (MIC90of ≤0.5 mg/liter). Ninety-six percent of fluoroquinolone-resistantP. aeruginosastrains were inhibited at a ceftazidime-avibactam MIC of ≤8 mg/liter (using the susceptible CLSI breakpoint for ceftazidime alone as a reference), with a MIC90of 8 mg/liter. Additionally, fluoroquinolone-resistant mutants from each species tested were obtainedin vitrofrom two strains, one susceptible to ceftazidime and the other a β-lactamase producer with a high MIC against ceftazidime but susceptible to ceftazidime-avibactam. Thereby, the impact of fluoroquinolone resistance on the activity of ceftazidime-avibactam could be assessed. The MIC90values of ceftazidime-avibactam for the fluoroquinolone-resistant mutant strains ofEnterobacteriaceaeandP. aeruginosawere ≤4 mg/liter and ≤8 mg/liter, respectively. We conclude that the presence of fluoroquinolone resistance does not affectEnterobacteriaceaeandP. aeruginosasusceptibility to ceftazidime-avibactam; that is, there is no cross-resistance.

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