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Biomedical subjects

S Normark

Publications and source records attributed to S Normark.

188 records · Page 11Linked to original sources
PubMed1969

Mutant of Escherichia coli with anomalous cell division and ability to decrease episomally and chromosomally mediated resistance to ampicillin and several other antibiotics.

In a mutation experiment with a rough, ampicillin-resistant strain, we isolated two smooth mutants which were both sensitive to ampicillin and carried defects in the cell envelope. One of the strains (with the envA gene) is hindered in its completion of septa and forms chains of cells. The envA gene has been mapped to a position between leu and proB, at 2 to 4 min. The envA gene decreased the resistance mediated by both episomal and chromosomal genes for resistance to several antibiotics. During growth the envA mutant was characterized by abnormal ratios between viable count or cell count and optical density. The ratio between viable count and optical density was affected during shift-up and shift-down experiments. When compared to the parent strain, the envA mutant was found to be more resistant to ultraviolet irradiation on plates. Prestarvation for tryptophan had a protective effect against irradiation both on the parent strain and the envA mutant.

Ampicillin↗
PubMed1969

Mutation in Escherichia coli K-12 mediating spherelike envelopes and changes tolerance to ultraviolet irradiation and some antibiotics.

In a mutation experiment with a rough, ampicillin-resistant strain of Escherichia coli K-12, two smooth ampicillin-sensitive mutants were isolated. One of the mutants (with the envA gene) was recently described. The second mutant (strain D23) with the envB gene which has been mapped to a position close to streptomycin resistance (strA) at 64 min is described. The envB gene gives rise to spherelike cells. Electron microscopy revealed an abnormal septum formation and a circular distribution of the nuclear material. Strain D23 (with envB) showed a changed resistance to several antibiotics as well as an increased tolerance to ultraviolet irradiation. The envB gene decreased the ampicillin resistance mediated by the ampA gene (at 82 min), but no effect was found on episomally mediated penicillin resistance.

Ampicillin↗
PubMedDate not supplied

Localization of the receptor-binding protein adhesin at the tip of the bacterial pilus.

Strains of the bacterium Escherichia coli that cause infections of the human urinary tract produce so-called Pap-pili, which are hair-like appendages consisting of about 10(3) helically arranged subunits of the protein PapA. These pili mediate binding to digalactoside-containing glycolipids present on the epithelial cells which line the urinary tract. Recently, it has been suggested that three proteins, PapE, PapF and PapG, are responsible for this binding. In the absence of PapA, non-piliated bacteria are formed which nonetheless exhibit binding, showing that the bulk of the pilus is not essential for binding. Although pili can form without PapF and PapG, such pili are unable to bind to the digalactoside. The protein PapG mediates binding specificity in trans-complementation experiments, so this protein is the digalactoside-specific adhesin. Using immuno-electron microscopy we have found that Pap-pili are heteropolymers composed of the major pilin, PapA, the minor pilins, PapE and PapF, and the adhesin, PapG. The last three proteins are located at the tip of the pilus.

Adhesins, Escherichia coli↗
PubMedDate not supplied

Genetic basis of induction and overproduction of chromosomal class I beta-lactamase in nonfastidious gram-negative bacilli.

Pseudomonas and several species of gram-negative enterobacteria produce low levels of chromosomally encoded class I beta-lactamase. The level of synthesis can be greatly increased by the addition of beta-lactam antibiotics into the growth medium. Moreover, mutants overproducing the enzyme arise at a high frequency in these species. The beta-lactamase is encoded by the chromosomal ampC gene, and its induction is governed by the ampR regulatory gene, which encodes an activator of ampC transcription. The ampD gene acts, probably indirectly, as a repressor of beta-lactamase synthesis, and it is in this gene that mutations leading to enzyme overproduction are located.

Chromosomes, Bacterial↗
PubMedDate not supplied

Contribution of chromosomal beta-lactamases to beta-lactam resistance in enterobacteria.

The two most important factors determining the level of beta-lactam resistance to novel cephalosporins in gram-negative enterobacteria are the chromosomal class C beta-lactamases, which have high affinity for these compounds, and the outer membrane permeability barrier. The individual importance of these factors and the interactions between them are discussed. Wild-type strains carry a chromosomal gene, ampC, encoding class C beta-lactamases. Expression from this gene is normally low, but it can in some species be induced by beta-lactam agents and related compounds. The current knowledge on the molecular mechanism governing both inducible and constitutive beta-lactamase synthesis is reviewed. Insight into these mechanisms explains why mutations leading to high-level enzyme over-production and beta-lactam resistance are much more frequent in species with a normally inducible beta-lactamase gene than in other gram-negative bacteria.

Anti-Bacterial Agents↗