Free-living and symbiotic characteristics of chlorate resistant mutants of Rhizobium japonicum

1980 ◽  
Vol 26 (3) ◽  
pp. 338-342 ◽  
Author(s):  
Laura de Vasconcelos ◽  
Llonas Miller ◽  
Carlos A. Neyra
Keyword(s):  
Nitrate Reductase ◽  
Parent Strain ◽  
Rhizobium Japonicum ◽  
Free Living ◽  
Chlorate Resistance ◽  
Soybean Seedlings ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Selection Of ◽  
Better Than

This work investigated the usefulness of chlorate resistance as a method for the selection of nitrate reductase negative (NR−) strains from Rhizobium japonicum (61A76) and evaluated the symbiotic characteristics of these strains. Chlorate resistant strains were selected from populations seeded on CS 7 agar containing 10 or 20 mM KClO3 and incubated in 2% air – 98% N2–CO2 (95:5).Over 200 resistant strains were isolated, 58% of which lacked the dissimilatory nitrate reductase. In 12 selected isolates, some strains had also lost the assimilatory nitrate reductase, but all retained hydrogenase activity.Chlorate resistant strains inoculated to soybean seedlings were equal to or better than the parent strain in terms of nodule mass and acetylene reduction. Those strains lacking both assimilatory and dissimilatory nitrate reductase showed the best symbiotic characteristics, suggesting that chlorate resistance in R. japonicum could be a useful method for the selection of strains with superior nitrogen-fixing characteristics.

scholarly journals Antipneumococcal Activities of Two Novel Macrolides, GW 773546 and GW 708408, Compared with Those of Erythromycin, Azithromycin, Clarithromycin, Clindamycin, and Telithromycin

2004 ◽  
Vol 48 (11) ◽  
pp. 4103-4112 ◽  
Author(s):  
Vlatka Matic ◽  
Klaudia Kosowska ◽  
Bulent Bozdogan ◽  
Linda M. Kelly ◽  
Kathy Smith ◽  
...  
Keyword(s):  
Ribosomal Protein ◽  
Protein Sequence ◽  
Single Step ◽  
23S Rrna ◽  
Susceptible Parent ◽  
Rrna Sequence ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Rrna Sequences ◽  
Selection Of

ABSTRACT The MICs of GW 773546, GW 708408, and telithromycin for 164 macrolide-susceptible and 161 macrolide-resistant pneumococci were low. The MICs of GW 773546, GW 708408, and telithromycin for macrolide-resistant strains were similar, irrespective of the resistance genotypes of the strains. Clindamycin was active against all macrolide-resistant strains except those with erm(B) and one strain with a 23S rRNA mutation. GW 773546, GW 708408, and telithromycin at two times their MICs were bactericidal after 24 h for 7 to 8 of 12 strains. Serial passages of 12 strains in the presence of sub-MICs yielded 54 mutants, 29 of which had changes in the L4 or L22 protein or the 23S rRNA sequence. Among the macrolide-susceptible strains, resistant mutants developed most rapidly after passage in the presence of clindamycin, GW 773546, erythromycin, azithromycin, and clarithromycin and slowest after passage in the presence of GW 708408 and telithromycin. Selection of strains for which MICs were ≥0.5 μg/ml from susceptible parents occurred only with erythromycin, azithromycin, clarithromycin, and clindamycin; 36 resistant clones from susceptible parent strains had changes in the sequences of the L4 or L22 protein or 23S rRNA. No mef(E) strains yielded resistant clones after passage in the presence of erythromycin and azithromycin. Selection with GW 773546, GW 708408, telithromycin, and clindamycin in two mef(E) strains did not raise the erythromycin, azithromycin, and clarithromycin MICs more than twofold. There were no change in the ribosomal protein (L4 or L22) or 23S rRNA sequences for 15 of 18 mutants selected for macrolide resistance; 3 mutants had changes in the L22-protein sequence. GW 773546, GW 708408, and telithromycin selected clones for which MICs were 0.03 to >2.0 μg/ml. Single-step studies showed mutation frequencies <5.0 × 10−10 to 3.5 × 10−7 for GW 773546, GW 708408, and telithromycin for macrolide-susceptible strains and 1.1 × 10−7 to >4.3 × 10−3 for resistant strains. The postantibiotic effects of GW 773546, GW 708408, and telithromycin were 2.4 to 9.8 h.

Selection of symbiotically energy efficient strains of Rhizobium japonicum by their ability to induce a H2-uptake hydrogenase in the free-living state

1981 ◽  
Vol 128 (3) ◽  
pp. 275-279 ◽  
Author(s):  
T. Ruiz-Argüeso ◽  
E. Cabrera ◽  
Mirta Barate de Bertalmio
Keyword(s):  
Energy Efficient ◽  
Rhizobium Japonicum ◽  
Uptake Hydrogenase ◽  
Free Living ◽  
Living State ◽  
Selection Of

scholarly journals In Vitro Activity of CEM-101 against Streptococcus pneumoniae and Streptococcus pyogenes with Defined Macrolide Resistance Mechanisms

2009 ◽  
Vol 54 (1) ◽  
pp. 230-238 ◽  
Author(s):  
Pamela McGhee ◽  
Catherine Clark ◽  
Klaudia M. Kosowska-Shick ◽  
Kensuke Nagai ◽  
Bonifacio Dewasse ◽  
...  
Keyword(s):  
Streptococcus Pyogenes ◽  
Bacterial Species ◽  
Resistance Mechanisms ◽  
Macrolide Resistance ◽  
23S Rrna ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
The One ◽  
Selection Of

ABSTRACT CEM-101 had MIC ranges of 0.002 to 0.016 μg/ml against macrolide-susceptible pneumococci and 0.004 to 1 μg/ml against macrolide-resistant phenotypes. Only 3 strains with erm(B), with or without mef(A), had CEM-101 MICs of 1 μg/ml, and 218/221 strains had CEM-101 MICs of ≤0.5 μg/ml. CEM-101 MICs were as much as 4-fold lower than telithromycin MICs against all strains. For Streptococcus pyogenes, CEM-101 MICs ranged from 0.008 to 0.03 μg/ml against macrolide-susceptible strains and from 0.015 to 1 μg/ml against macrolide-resistant strains. Against erm(B) strains, erythromycin, azithromycin, and clarithromycin MICs were 32 to >64 μg/ml, while 17/19 strains had telithromycin MICs of 4 to 16 μg/ml; CEM-101 MICs were 0.015 to 1 μg/ml. By comparison, erm(A) and mef(A) strains had CEM-101 MICs of 0.015 to 0.5 μg/ml, clindamycin and telithromycin MICs of ≤1 μg/ml, and erythromycin, azithromycin, and clarithromycin MICs of 0.5 to >64 μg/ml. Pneumococcal multistep resistance studies showed that although CEM-101 yielded clones with higher MICs for all eight strains tested, seven of eight strains had clones with CEM-101 MICs that rose from 0.004 to 0.03 μg/ml (parental strains) to 0.06 to 0.5 μg/ml (resistant clones); for only one erm(B) mef(A) strain with a parental MIC of 1 μg/ml was there a resistant clone with a MIC of 32 μg/ml, with no detectable mutations in the L4, L22, or 23S rRNA sequence. Among two of five S. pyogenes strains tested, CEM-101 MICs rose from 0.03 to 0.25 μg/ml, and only for the one strain with erm(B) did CEM-101 MICs rise from 1 to 8 μg/ml, with no changes occurring in any macrolide resistance determinant. CEM-101 had low MICs as well as low potential for the selection of resistant mutants, independent of bacterial species or resistance phenotypes in pneumococci and S. pyogenes.

Latent infections in avian malaria in relation to the production of drug-resistance

Parasitology ◽  
1951 ◽  
Vol 41 (1-2) ◽  
pp. 110-116 ◽  
Author(s):  
Elspeth W. McConnachie
Keyword(s):  
Drug Resistance ◽  
Avian Malaria ◽  
Latent Infection ◽  
Prolonged Treatment ◽  
Reproduction Rate ◽  
Latent Infections ◽  
Once Daily ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Selection Of

1. No resistance to paludrine or to sulphadiazine was obtained after treating latent infections of Plasmodium gallinaceum in chickens with twice daily doses of 20 mg./20 g. of sulphadiazine over periods of 171, 178 and 190 days.2. No resistance to paludrine was obtained after treating a latent infection of P. relictum in a canary over a period of 1 year with doses of paludrine increasing from 0·05 mg./20 g. once daily to 1·0 mg./ 20 g. twice daily.3. It is considered that if drug-resistance arises by mutation and selection, then resistance should arise more readily when a large number of rapidly multiplying parasites is treated with a drug than when the population treated is small, with a low reproduction rate, i.e. the failure to obtain resistant strains of malaria by prolonged treatment of latent infections with large amounts of drug, lends support to the theory of the origin of resistant strains of malaria by the selection of resistant mutants.

Selection of a BHC-resistant Strain of Drosophila melanogaster Mg

1953 ◽  
Vol 44 (2) ◽  
pp. 395-400 ◽  
Author(s):  
F. J. Oppenoorth ◽  
D. Dresden
Keyword(s):  
Drosophila Melanogaster ◽  
Resistant Strain ◽  
Parent Strain ◽  
Laboratory Strain ◽  
Contact Method ◽  
Resistant Parent ◽  
Reciprocal Crosses ◽  
Wild Strains ◽  
Resistant Strains ◽  
Selection Of

Two wild strains of Drosophila and one laboratory strain were selected for resistance to γBHC by a contact method. From each of these three strains equally resistant strains developed in about the same time. They did not become more resistant after prolonged selection. The resistance obtained was further investigated in one of the strains.There was no evidence of any specificity: the susceptibility of the resistant insects to DDT and “Thanite” also appeared to be less than that of the original strains.Although the strains were selected by a contact method they also showed decreased susceptiblity when the poison was applied to the skin and when it was injected. From the reciprocal crosses F1's were obtained the susceptibilities of which were practically the same and differed little from that of the resistant parent strain. It follows that resistance does not depend on cytoplasmatic heredity and that it is incompletely dominant.

scholarly journals Fluoroquinolone Action against Mycobacteria: Effects of C-8 Substituents on Growth, Survival, and Resistance

1998 ◽  
Vol 42 (11) ◽  
pp. 2978-2984 ◽  
Author(s):  
Yuzhi Dong ◽  
Chen Xu ◽  
Xilin Zhao ◽  
John Domagala ◽  
Karl Drlica
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Bacterial Species ◽  
Resistant Mutant ◽  
Methoxyl Group ◽  
Bacteriostatic Activity ◽  
Dna Breaks ◽  
Lethal Action ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Selection Of

ABSTRACT Fluoroquinolones trap gyrase on DNA as bacteriostatic complexes from which lethal DNA breaks are released. Substituents at the C-8 position increase activities of N-1-cyclopropyl fluoroquinolones against several bacterial species. In the present study, a C-8-methoxyl group improved bacteriostatic action againstgyrA (gyrase-resistant) strains ofMycobacterium tuberculosis and M. bovis BCG. It also enhanced lethal action against gyrase mutants of M. bovis BCG. When cultures of M. smegmatis, M. bovis BCG, and M. tuberculosis were challenged with a C-8-methoxyl fluoroquinolone, no resistant mutant was recovered under conditions in which more than 1,000 mutants were obtained with a C-8-H control. A C-8-bromo substituent also increased bacteriostatic and lethal activities against a gyrA mutant of M. bovisBCG. When lethal activity was normalized to bacteriostatic activity, the C-8-methoxyl compound was more bactericidal than its C-8-H control, while the C-8-bromo fluoroquinolone was not. The C-8-methoxyl compound was also found to be more effective than the C-8-bromo fluoroquinolone at reducing selection of resistant mutants when each was compared to a C-8-H control over a broad concentration range. These data indicate that a C-8-methoxyl substituent, which facilitates attack of first-step gyrase mutants, may help make fluoroquinolones effective antituberculosis agents.

scholarly journals Cefotaxime Acts Synergistically with Levofloxacin in Experimental Meningitis Due to Penicillin-Resistant Pneumococci and Prevents Selection of Levofloxacin-Resistant Mutants In Vitro

2003 ◽  
Vol 47 (8) ◽  
pp. 2487-2491 ◽  
Author(s):  
F. Kühn ◽  
M. Cottagnoud ◽  
F. Acosta ◽  
L. Flatz ◽  
J. Entenza ◽  
...  
Keyword(s):  
Induced Resistance ◽  
Fold Increase ◽  
Low Doses ◽  
Topoisomerase Iv ◽  
Pneumococcal Strain ◽  
Genes Encoding ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Selection Of

ABSTRACT Cefotaxime, given in two doses (each 100 mg/kg of body weight), produced a good bactericidal activity (−0.47 Δlog10 CFU/ml · h) which was comparable to that of levofloxacin (−0.49 Δlog10 CFU/ml · h) against a penicillin-resistant pneumococcal strain WB4 in experimental meningitis. Cefotaxime combined with levofloxacin acted synergistically (−1.04 Δlog10 CFU/ml · h). Synergy between cefotaxime and levofloxacin was also demonstrated in vitro in time killing assays and with the checkerboard method for two penicillin-resistant strains (WB4 and KR4). Using in vitro cycling experiments, the addition of cefotaxime in sub-MIC concentrations (one-eighth of the MIC) drastically reduced levofloxacin-induced resistance in the same two strains (64-fold increase of the MIC of levofloxacin after 12 cycles versus 2-fold increase of the MIC of levofloxacin combined with cefotaxime). Mutations detected in the genes encoding topoisomerase IV (parC and parE) and gyrase (gyrA and gyrB) confirmed the levofloxacin-induced resistance in both strains. Addition of cefotaxime in low doses was able to suppress levofloxacin-induced resistance.

Rifamycin-Resistant Mutation in E. coli: Effect of Rifamycin on DNA-Dependent RNA Polymerase and on R17 Phage Growth

1972 ◽  
Vol 50 (2) ◽  
pp. 128-135
Author(s):  
S. J. Igarashi
Keyword(s):  
Rna Polymerase ◽  
Template Molecule ◽  
E Coli ◽  
Resistant Strains ◽  
Resistant Mutants ◽  
Natural Mutation ◽  
Male Specific ◽  
Phage Growth ◽  
Resistant Mutation ◽  
Selection Of

Rifamycin-resistant mutants in E. coli, K12, Hfr strain, were isolated without mutagenic treatment. The frequency of natural mutation of this type appeared to be approximately 10−9. Selection of resistant strains was effected by plating 109 cells on agar plates containing 50 μg of rifamycin per milliliter. A total of 11 strains resistant to rifamycin thus isolated remained Hfr and, in the presence of rifamycin, permitted the growth of the RNA-containing, male specific coliphage R17, which is sensitive to rifamycin in a wild-type E. coli. DNA-dependent RNA polymerase was prepared from these resistant mutants and examined for sensitivity toward rifamycin and other antibiotics. It was found that the RNA polymerase of the resistant strain is indeed resistant to rifamycin. However, both rifamycin-resistant and -sensitive enzymes are inhibited by the other three antibiotics (acridine orange, ethidium bromide, actinomycin D), which are known to interact with the template molecule.

Determination of the distribution of three nitrate reductase isoforms in soybean seedlings by chromatography and a simple method based on assay conditions

1992 ◽  
Vol 85 (3) ◽  
pp. 541-548 ◽  
Author(s):  
Nicole Cathala ◽  
Genevieve Conejero ◽  
Alain Gojon ◽  
Lucien Passama ◽  
Paul Robin
Keyword(s):  
Nitrate Reductase ◽  
Simple Method ◽  
Soybean Seedlings ◽  
Assay Conditions
Sign in / Sign up

Export Citation Format

Share Document