scholarly journals A genetic analysis of resistance to nystatin inSaccharomyces cerevisiae

1967 ◽  
Vol 9 (2) ◽  
pp. 179-193 ◽  
Author(s):  
K. A. Ahmed ◽  
R. A. Woods

1. A number of stable nystatin-resistant mutants of the yeastSaccharomyces cerevisiaehave been isolated from platings of a sensitive wild-type strain on low concentrations of the antibiotic.2. These mutants were found to be resistant to 10, 15 or 60 units of drug/ml.3. Analysis of meiotic segregants from crosses of these mutants to wild-type indicate that resistance is determined by two types of genes; resistance genes and modifiers.4. Functional analysis of the mutants demonstrated the existence of three recessive resistance genes,nys-l,nys-2 andnys-3 and thatnys-1 andnys-2 were linked.5. Genetic analysis showed thatnys-1 was affected by two modifiers,Mnys-1 andMnys-2, but that onlyMnys-2 affectednys-2 andnys-3.6. The modifiersMnys-1 andMnys-2 are dominant.7. An investigation of the effects of temperature and medium on resistance demonstrated marked interactions between genotype and environment for both the resistance genes and the modifiers.8. Second-step mutants have been isolated by plating first-step mutants on higher concentrations of the drug. Some of these are resistant to 800 units/ml.9. Some possible mechanisms of nystatin resistance are discussed.

2006 ◽  
Vol 50 (2) ◽  
pp. 445-452 ◽  
Author(s):  
Daniel Criswell ◽  
Virginia L. Tobiason ◽  
J. Stephen Lodmell ◽  
D. Scott Samuels

ABSTRACT We have isolated and characterized in vitro mutants of the Lyme disease agent Borrelia burgdorferi that are resistant to spectinomycin, kanamycin, gentamicin, or streptomycin, antibiotics that target the small subunit of the ribosome. 16S rRNA mutations A1185G and C1186U, homologous to Escherichia coli nucleotides A1191 and C1192, conferred >2,200-fold and 1,300-fold resistance to spectinomycin, respectively. A 16S rRNA A1402G mutation, homologous to E. coli A1408, conferred >90-fold resistance to kanamycin and >240-fold resistance to gentamicin. Two mutations were identified in the gene for ribosomal protein S12, at a site homologous to E. coli residue Lys-87, in mutants selected in streptomycin. Substitutions at codon 88, K88R and K88E, conferred 7-fold resistance and 10-fold resistance, respectively, to streptomycin on B. burgdorferi. The 16S rRNA A1185G and C1186U mutations, associated with spectinomycin resistance, appeared in a population of B. burgdorferi parental strain B31 at a high frequency of 6 × 10−6. These spectinomycin-resistant mutants successfully competed with the wild-type strain during 100 generations of coculture in vitro. The aminoglycoside-resistant mutants appeared at a frequency of 3 × 10−9 to 1 ×10−7 in a population and were unable to compete with wild-type strain B31 after 100 generations. This is the first description of mutations in the B. burgdorferi ribosome that confer resistance to antibiotics. These results have implications for the evolution of antibiotic resistance, because the 16S rRNA mutations conferring spectinomycin resistance have no significant fitness cost in vitro, and for the development of new selectable markers.


1974 ◽  
Vol 23 (3) ◽  
pp. 335-359 ◽  
Author(s):  
Joan L. Betz ◽  
Jane E. Brown ◽  
Patricia H. Clarke ◽  
Martin Day

SUMMARYMutants ofPseudomonas aeruginosa, which differed in amide growth phenotype from the wild-type strain, were subjected to genetic analysis using the generalized transducing phage F116. The map order of some mutational sites was determined by 3-factor crosses in which a mutation in the linked regulator geneamiRwas used as the outside marker to determine the relative order of mutations in the amidase structural geneamiE. Acetamide-positive transductants were recovered in crosses between amidase-negative strains and strains PhB3(PAC377), V2(PAC353) and V5(PAC356) producing mutant amidases which hydrolyse phenylacetamide and valeramide but not acetamide. Some recombinants carried the mutationamiE16 determining the properties of the mutant B amidase produced by strain B6(PAC351) from which both PhB and V class mutants were derived, while other recombinants produced A amidase determined by the wild-typeamiEgene.


1982 ◽  
Vol 60 (1) ◽  
pp. 79-84 ◽  
Author(s):  
A. Babai-Ahary ◽  
M. J. Daboussi-Bareyre ◽  
D. Parisot

Mutants with altered sexual reproduction were isolated from a homothallic wild-type strain of Nectria haematococca (Berk. & Br.) Wr. and genetically analysed. Most were self- and inter-sterile but some were interfertile and were used to improve genetic analysis by allowing an easy detection of hybrid perithecia. The study of these mutants also provides information about various aspects of the perithecial development in this organism.


2003 ◽  
Vol 47 (5) ◽  
pp. 1560-1564 ◽  
Author(s):  
G. Plantefeve ◽  
H. Dupont ◽  
V. Hubert ◽  
L. Garry ◽  
C. Poüs ◽  
...  

ABSTRACT The relationship between virulence and chromosomal elements containing glycopeptide resistance genes was experimentally assessed for two transconjugant strains of Enterococcus faecalis (VanA and VanB phenotypes) and compared to that for a susceptible wild-type strain. Microbiologic and inflammatory effects were assessed in a polymicrobial rat model of peritonitis. Mean peritoneal enterococcus concentrations ± standard deviations at day 1 were 2.1 ± 1.9, 1.3 ± 1.1, and 1.7 ± 2.0 log10 CFU/ml for susceptible, VanA, and VanB strains, respectively (P < 0.05). At day 3 also there were lower concentrations of glycopeptide-resistant enterococcal strains in peritoneal fluid (3.2 ± 3.4, 1.8 ± 1.8, and 2.1 ± 2.4 log10 CFU/ml for susceptible, VanA, and VanB strains, respectively [P < 0.05]). Transconjugant glycopeptide-resistant strains were associated with increased peritoneal cell counts at the different evaluation times of the experiment (P < 0.001). Plasma α1-acid glycoprotein concentrations were lower in the presence of the susceptible strain (667 ± 189 mg/liter) than in the presence of the VanA or VanB strain (1,193 ± 419 or 1,210 ± 404 mg/liter, respectively [P < 0.05]), while concentrations of tumor necrosis factor alpha and interleukin-6 in peritoneal fluid remained similar for the strains. These results suggest a trend toward variation of virulence of transconjugant strains compared to the wild-type strain in this peritonitis model.


2004 ◽  
Vol 48 (8) ◽  
pp. 3203-3206 ◽  
Author(s):  
George A. Jacoby ◽  
Debra M. Mills ◽  
Nancy Chow

ABSTRACT High-level resistance to ertapenem was produced by β-lactamases of groups 1, 2f, and 3 in a strain of Klebsiella pneumoniae deficient in Omp35 and Omp36. From a wild-type strain producing ACT-1 β-lactamase, ertapenem-resistant mutants for which the ertapenem MICs were up to 128 μg/ml and expression of outer membrane proteins was diminished could be selected.


2000 ◽  
Vol 182 (18) ◽  
pp. 5278-5279 ◽  
Author(s):  
Yasurou Kurusu ◽  
Tomoaki Narita ◽  
Makoto Suzuki ◽  
Taeko Watanabe

ABSTRACT We genetically characterized the Pseudomonas putida mutS gene and found that it encodes a smaller MutS protein than do the genes of other bacteria. This gene is able to function in themutS mutants of Escherichia coli andBacillus subtilis. A P. putida mutS mutant has a mutation frequency 1,000-fold greater than that of the wild-type strain.


1999 ◽  
Vol 37 (9) ◽  
pp. 2913-2919 ◽  
Author(s):  
Robert Morse ◽  
Karen O’Hanlon ◽  
Mumtaz Virji ◽  
Matthew D. Collins

The sequence of the rpoB gene from Listeria monocytogenes was determined. Rifampin-resistant (Rifr) mutants arising from L. monocytogenes cultures exposed to rifampin were isolated, and by partial sequencing of their rpoB genes, seven different point mutations affecting five different amino acids (473Asp→Asn or Gly, 479Gly→Asp, 483His→Tyr or Leu, 528Ile→Phe, and 530Ser→Tyr), which led to MICs of 0.5 to 100 μg/ml for the organisms, were determined. These mutants showed various deficiencies for growth at 42°C, with only one being comparable to the wild-type strain. The interaction of these Rifr mutants with human Caco-2 cells was examined by using an immunofluorescence technique. Three mutants failed to interact, while three showed a reduced interaction compared to that of the wild type. It is believed that these pleiotropic phenotypes have arisen as a result of mutations within the DNA-dependent RNA polymerase holoenzyme.


Microbiology ◽  
2004 ◽  
Vol 150 (5) ◽  
pp. 1327-1338 ◽  
Author(s):  
Andrea M. Smania ◽  
Ignacio Segura ◽  
Roberto J. Pezza ◽  
Cecilia Becerra ◽  
Inés Albesa ◽  
...  

MutS is part of the bacterial mismatch repair system that corrects point mutations and small insertions/deletions that fail to be proof-read by DNA polymerase activity. In this work it is shown that the disruption of the P. aeruginosa mutS gene generates the emergence of diverse colony morphologies in contrast with its parental wild-type strain that displayed monomorphic colonies. Interestingly, two of the mutS morphotypes emerged at a high frequency and in a reproducible way and were selected for subsequent characterization. One of them displayed a nearly wild-type morphology while the other notably showed, compared with the wild-type strain, increased production of pyocyanin and pyoverdin, lower excretion of LasB protease and novel motility characteristics, mainly related to swarming. Furthermore, it was reproducibly observed that, after prolonged incubation in liquid culture, the pigmented variant consistently emerged from the mutS wild-type-like variant displaying a reproducible event. It is also shown that these P. aeruginosa mutS morphotypes not only displayed an increase in the frequency of antibiotic-resistant mutants, as described for clinical P. aeruginosa mutator isolates, but also generated mutants whose antibiotic-resistant levels were higher than those measured from spontaneous resistant mutants derived from wild-type cells. It was also found that both morphotypes showed a decreased cytotoxic capacity compared to the wild-type strain, leading to the emergence of invasive variants. By using mutated versions of a tetracycline resistance gene, the mutS mutant showed a 70-fold increase in the reversion frequency of a +1 frameshift mutation with respect to its parental wild-type strain, allowing the suggestion that the phenotypical diversity generated in the mutS population could be produced in part by frameshift mutations. Finally, since morphotypical diversification has also been described in clinical isolates, the possibility that this mutS diversification was related to the high frequency hypermutability observed in P. aeruginosa CF isolates is discussed.


Genetics ◽  
1976 ◽  
Vol 82 (4) ◽  
pp. 645-663
Author(s):  
Philip S Perlman

ABSTRACT We have studied a number of petite [rho  -] mutants of Saccharomyces cerevisiae induced in a wild-type strain of mitochondrial genotype [ome  -  CHLR ERYS OLIS  1,2,3 PARS] by Berenil and ethidium bromide, all of which have retained two mitochondrial genetic markers, [CHLR] and [ERYS], but have lost all other known markers. Though stable in their ability to retain these markers in their genome, these mutants vary widely among themselves in suppressiveness and in the extent to which the markers are transmitted on crossing to a common wild-type tested strain. In appropriate crosses all of the strains examined in this study demonstrate mitochondrial polarity, and thus have also retained the [ome  -] locus in a functional form; however, five different transmissional types were obtained, several of them quite unusual, particularly among the strains originally induced by Berenil. One of the most interesting types is the one that appears to reverse the parental genotypes with [CHLR ERYS] predominating over [CHLS ERYR] in the diploid [rho+] progeny, rather than the reverse, which is characteristic of analogous crosses with [rho+] or other petites. Mutants in this class also exhibited low or no suppressiveness. Since all of the petites reported here are derived from the same wild-type parent, and so have the same nuclear background, we have interpreted the transmissional differences as being due to different intramolecular arrangements of largely common retained sequences.


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