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At least 199 records · Page 11Linked to original sources

PubMed1970

Effect of chloramphenicol on host-bacteriophage relationships in the lactic streptococci.

Chloramphenicol (CM)-resistant mutants of Streptococcus lactis strain ML3 were obtained either as a consequence of continuous transfer of the bacteria in broth containing increasing amounts of CM or by selecting for high-level resistant derivatives after mutagenic treatment of the bacteria. Some CM-resistant cells obtained by the first method were also resistant to the homologous bacteriophage. Cells trained to grow in the presence of CM developed resistance to some heterologous attacking phages but not to phage ml(3). Mutants selected for phage resistance were not resistant to CM. There appear to be two different loci for CM resistance on the bacterial chromosome: the one for high-level resistance is associated with the phage-resistance locus and the other is independent of it. A concentration of CM (280 mug/ml) that was bacteriostatic for ML3 inhibited the intracellular growth of ml(3) phage in strain ML3-CM(r)I, which had been trained to grow in the presence of that CM concentration, despite the fact that cells of this strain were not phage-resistant per se. The drug had no direct virucidal action and did not prevent adsorption to or penetration of phage into the bacterium. Lysogenization did not occur. It is concluded that the block in phage development probably involves inhibition of synthesis of phage components, either involving deoxyribonucleic acid at an early stage or the phage coat protein at a later one.

Bacteriophages↗

PubMed1970

Susceptibility of Pseudomonas aeruginosa to gentamicin sulfate in vitro: lack of correlation between disc diffusion and broth dilution sensitivity data.

Seventy-eight of 420 clinical isolates of Pseudomonas aeruginosa yielded zones of inhibition of less than 12 mm in diameter around 10-mug discs of gentamicin sulfate when tested by the standardized Bauer-Kirby disc diffusion method. Of 153 strains chosen from these isolates, one strain (0.65%) required 25 mug of gentamicin per ml for inhibition; the remainder (99.35%) were inhibited by 6 mug/ml or less of the antibiotic. It is recommended that those isolates of P. aeruginosa that yield zones of inhibition less than 12 mm in diameter be disc susceptibility-tested once more; those isolates that give zones of inhibition of less than 12 mm upon repeated examination should then be subjected to the broth dilution test before they are designated as sensitive or resistant to gentamicin.

Agar↗

PubMed1971

Resistance to D-cycloserine in the tubercle bacilli: mutation rate and transport of alanine in parental cells and drug-resistant mutants.

A single transport system was found to accumulate l- and d-alanine, glycine and d-serine in Mycobacterium tuberculosis. The results of inhibition experiments suggested that the antibiotics d-cycloserine and O-carbamyl-d-serine were also transported by the alanine-glycine-d-serine system. A d-cycloserine-resistant permease-competent (d-CS(r)/perm(+)) mutant and a d-cycloserine-resistant permease-defective (d-CS(r)/perm(-)) mutant were isolated. The d-CS(r)/perm(-) mutant was not found to be more resistant to the drug than was the d-CS(r)/perm(+) mutant. The data were consistent with the conclusion that resistance to d-cycloserine in the tubercle bacilli is primarily due to mutations in the gene(s) controlling the enzyme d-alanyl-d-alanine synthetase. The mutation rate was calculated to be about 10(-10) mutations per bacterium per generation.

Alanine↗

PubMed1971

Effects of actinobolin on growth and some metabolic activities of cariogenic streptococci in vitro and in vivo.

Actinobolin, a known inhibitor of protein synthesis, has been shown not to interfere selectively with acid production or dextransucrase activity in a cariogenic streptococcus when the antibiotic is added to a concentration of 500 mug/ml. It has also been shown that actinobolin does not alter the total in vivo flora of the oral cavity of the rat when tested in a rat caries model system. A culture of cariogenic streptococci, adapted to in vitro growth in the presence of 1 mg of actinobolin per ml, has also been isolated.

Animals↗

PubMed1994

DNA fingerprinting of medically important microorganisms by use of PCR.

Selected segments of any DNA molecule can be amplified exponentially by PCR. This technique provides a powerful tool to detect and identify minimal numbers of microorganisms. PCR is applicable both in diagnosis and in epidemiology. By amplification of hypervariable DNA domains, differences can be detected even among closely related strains. PCR fingerprinting is a valuable tool for medical microbiologists, epidemiologists, and microbial taxonomists. The current state of PCR-mediated genotyping is reviewed, and a comparison with conventional molecular typing methods is included. Because of its speed and versatility, PCR fingerprinting will play an important role in microbial genetics, epidemiology, and systematics.

Animals↗

PubMed1971

Electron microscopy of the altered spore morphology of a ribonucleic acid polymerase mutant of Bacillus subtilis.

Electron microscopy was used to analyze sporulating cells and spores of Bacillus subtilis mutants (Rif(r)) which are resistant to rifampin, an inhibitor of ribonucleic acid polymerase. The spores of Rif-18 are pleomorphic and frequently exhibit terminal knobs. These knobs first occur during late stage IV and early stage V of sporulation and are extensions of the inner and outer spore coats. Since the rifampin resistance and altered spore morphology of Rif-18 are 100% cotransformable, these data suggest that the altered spore morphology is the result of an alteration in ribonucleic acid polymerase genes. The morphology and physical dimensions are also reported for spores from Rif-11, Rif-15, and Rif-21. Significant differences in size from the wild type were observed for these mutants.

Bacillus subtilis↗

PubMed1971

Mechanism of action of rifampin on Mycobacterium smegmatis.

Deoxyribonucleic acid (DNA)-dependent ribonucleic acid (RNA) polymerase (EC 2.7.7.6) isolated from a rifampin-sensitive strain of Mycobacterium smegmatis was 90% inhibited by 1 mug of rifampin per ml; enzyme from a rifampin-resistant mutant was not affected by this concentration of antibiotic. Inhibition of phenylalanine-1-(14)C incorporation by rifampin in growing cultures was complete about 6 min after addition of antibiotic. Under the same conditions, uracil-2-(14)c incorporated was blocked after 1.5 to 2 min. Rifampin kills M. smegmatis very slowly. When rifampin-inhibited cultures were transferred to a rifampin-free medium, there was a partial resumption of uracil-2-(14)C incorporation, even in the presence of chloramphenicol. We conclude that a primary event in the inhibition of M. smegmatis by rifampin is the block of DNA-dependent RNA polymerase.

Adenosine Monophosphate↗

PubMed1971

Pigmentation and acriflavine resistance in Serratia marcescens.

Stable, orange, acriflavine-resistant variants were selected by treatment of a wild-type, red, acriflavine-sensitive strain of Serratia marcescens with acriflavine. Visible, ultraviolet, infrared, and nuclear magnetic resonance spectra of purified pigment from the red strain were identical to those of the pigment from the orange strain, and the orange mutant was not due to a mutation affecting the structure of the pigment, prodigiosin. The color of the red strain was not affected by variations in pH between 5.0 and 8.0, whereas the color of the orange mutant changed from pink to orange over the same pH range. This variation was mimicked by the pH-induced variation in color of prodigiosin purified from either the red, wild-type or the orange, mutant strains. Density-gradient centrifugation of cell fragments after ultrasonic disintegration resulted in characteristic pigmented bands. Biochemical characterization of these pigmented bands showed that they contained pigment and a protein component, but no lipids, polysaccharides, sugars, glucosamine, or phosphates were detected. Further fractionation of these pigmented bands by zone electrophoresis on a sucrose density gradient indicated that some pigment in S. marcescens was specifically attached to protein components.

Acridines↗

PubMed1971

Effects of ethidium bromide on growth and on loss of the penicillinase plasmid of Staphylococcus aureus.

Ethidium bromide (EB) was more efficient than ethyl violet or rifampin as a curing agent for the penicillinase plasmids of Staphylococcus aureus strains. The effects of EB on growth and on the loss of the penicillinase plasmid of PS 81 were studied in detail. The growth rates of PS 81 and an EB-cured derivative were identical in broth, but the cured derivative had a shorter lag in the presence of added 6 x 10(-6)m EB. The shortened lag was due to prior exposure to EB as the cured derivative and an EB-treated but uncured strain of PS 81 gave identical growth lag and growth rates in the presence of EB. The curing of PS 81 by EB occurs in three phases. After a 4 to 5 hr lag, there is a 100-fold increase in the number of penicillinase-negative cells, and the proportion of cured cells continues to rise until 10 to 12 hr. Thereafter, the population becomes refractory to further curing, and the proportion of penicillinase-negative cells remains constant at about 20% of the total. Penicillinase-positive survivors of EB treatment showed increased EB resistance and were cured at lower rates upon subsequent EB treatment. Isolated colonies of the parental strain PS 81 were heterogeneous in their EB sensitivity. Thus, EB does not competitively favor spontaneously cured penicillinase-negative cells but appears to act in a manner analogous to acridine orange on the plasmids of enteric bacteria.

Coloring Agents↗

PubMed1972

Ureidosuccinic acid uptake in yeast and some aspects of its regulation.

Ureidosuccinic acid (USA) is an intermediary product in pyrimidine biosynthesis. When proline was the sole nitrogen source, USA uptake occurred; however, when ammonium sulfate or glutamic acid was the nitrogen source, uptake was inhibited. Thus, a ura2 strain which does not synthesize USA would not grow when this substance was supplied on an ammonium sulfate or glutamic acid medium. Mutants are described in which uptake was constitutive on such a medium. Permeaseless mutants for USA have been found, and evidence is presented for permease specificity. It is shown that all constitutive mutants use the same transport system that is missing in the permeaseless mutant. These mutants are constitutive for two permeases: the specific USA permease and the general amino acid permease. The transport system studied here, like the general amino acid transport system, is regulated by nitrogen metabolism. These facts and others suggest that our permease constitutive mutants are impaired in nitrogen metabolism.

Amino Acids↗

PubMed1972

Loss of the penicillinase plasmid after treatment of Staphylococcus aureus with sodium dodecyl sulfate.

Two strains of Staphylococcus aureus (PC1 and 196E), when grown in medium containing 0.002% sodium dodecyl sulfate (SDS), showed from 96.1 to 100% loss of the ability to produce penicillinase. Resistance to cadmium and zinc was lost concomitantly with the ability to produce penicillinase. A comparison of the rate of curing by SDS with the curing effects exerted by elevated temperature and ethidium bromide suggested that SDS is a more effective plasmid curing agent for susceptible strains of S. aureus than methods in use at present.

Cadmium↗

PubMed1972

Induction of cycloheximide-resistant mutants in Saccharomyces cerevisiae with N-methyl-N'-nitro-N-nitrosoguanidine and ICR-170.

N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG) induces cycloheximide-resistant mutations in Saccharomyces cerevisiae, but few, if any, resistant mutants are induced by the acridine mustard ICR-170. Cycloheximide sensitivity in yeast is associated with the ribosome, and treatment with the antibiotic at concentrations of 2 mug/ml results in complete inhibition of protein synthesis. Missense mutations induced by MNNG probably lead to the loss of cycloheximide binding sites on the ribosome, resulting in resistance to the antibiotic without altering the activity of the organelle in protein synthesis. ICR-170, however, induced primarily frameshift mutations that would alter ribosome structural integrity, resulting in cell death rather than resistance. ICR-170 and MNNG are both mutagenic in a system in which base-pair substitution and frameshift mutations can be detected. These results indicate that cycloheximide resistance in S. cerevisiae, like streptomycin and spectinomycin resistance in Escherichia coli, can be induced by base-pair substitution mutagens but not by frameshift mutagens such as ICR-170.

Acridines↗

PubMed1972

Interactions between amino acid transport systems in Neurospora crassa.

Mutants of Neurospora crassa, selected as resistant to l-canavanine and l-thialysine, are partially deficient in the uptake of basic amino acids. Neutral amino acids completely inhibit uptake of basic amino acids, and this inhibition is dependent on the activity of a neutral amino acid permease. In contradistinction, mutants resistant to 4-methyl-dl-tryptophan are partially deficient in the uptake of neutral amino acids. Basic amino acids completely inhibit neutral amino acid uptake, and this inhibition is dependent on the activity of a basic amino acid permease. It is proposed that these specific transport systems compete with a general amino acid permease for some common element. The general permease is also regulated by ammonia, the amino acid pool, or both. The activity of the general permease can be eliminated phenotypically by a high concentration of glycerol or a high temperature. It is also shown that l-citrulline is transported by the neutral amino acid permease and by the general amino acid permease.

Amino Acids↗

PubMed1968

Defective guanine uptake in an 8-azaguanine-resistant mutant of Salmonella typhimurium.

An 8-azaguanine-resistant mutant, azg-11, derived from a guanine auxotroph, gua-1, of Salmonella typhimurium was isolated. This mutant was resistant to the analogue when grown on 2,6-diaminopurine, but showed greater susceptibility than the parent on guanine. Studies with the uptake of radioactive purines revealed that the mutant was defective in a mechanism for incorporation of guanine as well as of xanthine. Initial rates of uptake were determined for guanine at concentrations which were sufficiently low to make permeases limiting. The affinity constant K(m) for the mutant was found to be 2.5 x 10(-4)m; that of the parent was 2.3 x 10(-5)m. Examination of cell-free extracts suggested that the purine nucleotide pyrophosphorylases, responsible for the conversion of free intracellular purines to the corresponding nucleotides, were present and unaltered. The results indicate that the mutant is defective in a mechanism for the active transport for guanine and possibly xanthine.

Adenine↗

PubMed1969

Interaction between analogue resistance and amino acid auxotrophy in Neurospora.

A new p-fluorophenylalanine resistant mutant of Neurospora (fpr-1) was isolated. It is unaffected by the suppressor of a previously described resistance mutant, mtr. The fpr-1 locus is on linkage group V, tightly linked to act-2. The expression of resistance to p-fluorophenylalanine by fpr-1 can be suppressed by genes controlling a requirement for lysine or arginine. The suppression seems to involve an increased sensitivity of the lysine and arginine auxotrophs to p-fluorophenylalanine.

Amino Acids↗

PubMed1971

Similar effect of rifampin and other rifamycin derivatives on vaccinia virus morphogenesis.

Membrane-limited structures, resembling virus envelope precursors previously shown to form during the interruption of poxvirus assembly by rifampin, were now observed by electron microscopy in vaccinia-infected HeLa cells treated with a series of rifamycin derivatives. The active compounds N-demethyl rifampin, AF/DMI, and 3-formyl rifamycin SV lacked, respectively, a methyl group, the piperazine ring, and the hydrazone portion of rifampin. A vaccinia mutant selected only for resistance to rifampin was also resistant to the effect on morphogenesis produced by all of the rifamycin derivatives. We concluded that this antiviral effect was specific and was a property associated with the macrocyclic ring rather than the hydrazone-containing side chain of rifampin. In addition to their effects on vaccinia morphogenesis, 3-formyl rifamycin SV and AF/DMI had unusual cytotoxic effects.

Anti-Bacterial Agents↗

PubMed1971

6(p-Hydroxyphenylazo)-uracil: a reversible, selective inhibitor of the replication of deoxyribonucleic acid of staphylococcal bacteriophage P11-M15.

6(p-Hydroxyphenylazo)-uracil (HPUra), a selective inhibitor of the semiconservative replication of deoxyribonucleic acid (DNA) of gram-positive bacteria, was found to inhibit the replication of DNA of bacteriophage P11-M15, a virulent derivative of the temperate Staphylococcus aureus bacteriophage P11. At appropriate concentration, HPUra inhibited DNA synthesis by P11-M15-infected S. aureus immediately and completely, regardless of the stage of the lytic cycle at which infected cells were exposed to drug. The effect of HPUra was reversible since the capacity of inhibited, infected cells to replicate phage DNA and produce mature phage could be restored by removal of HPUra from incubation media. Concentrations of HPUra which completely inhibited the replication of P11-M15 in its drug-sensitive host did not inhibit the replication of this phage or its DNA in several drug-resistant host mutants. HPUra also did not inhibit the replication of two other serologically distinct, virulent staphylococcal bacteriophages, P1 and 44AHJD, in drug-sensitive hosts.

Adenine↗

PubMed1983

Neoplastic conversion of preneoplastic Syrian hamster cells: rate estimation by fluctuation analysis.

Analysis of the role of gene mutations in the multistep process of neoplastic transformation requires that the discrete steps in carcinogenesis first be dissected. Toward this end, we have isolated and characterized preneoplastic Syrian hamster cells which exhibit in vitro a trait highly correlated with neoplastic conversion in vivo. Previous findings (J. C. Barrett, Cancer Res. 40:91-94, 1980) indicate that spontaneous neoplastic transformation of Syrian hamster cells occurs in at least two steps. An intermediate stage, characterized by an aneuploid established cell line which has a propensity to become neoplastic spontaneously upon further growth in vitro, has been described. These preneoplastic cells differ from diploid early-passage Syrian hamster cells in becoming capable of anchorage-independent growth in semisolid agar, as well as becoming neoplastic in vivo when attached to a solid substrate. Evidence presented here demonstrates that anchorage-independent conversion in vitro is a reliable marker for neoplastic conversion in this cell system. Fluctuation analyses, patterned after those described by Luria and Delbruck for microbial genetics, demonstrate that anchorage-independent variants are generated randomly from clonally derived preneoplastic cells at the rate of 10(-8) to 10(-7) variants per cell per generation. These results establish a multistep stochastic process for transformation in vitro and indicate that conversion to anchorage independence may be necessary for Syrian hamster cells to become tumorigenic. The possible role of gene mutation in this step during neoplastic progression is discussed.

Aneuploidy↗