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J D Hopkins

Publications and source records attributed to J D Hopkins.

25 records · Page 2Linked to original sources
PubMed1983

New class of mutations in Escherichia coli (uup) that affect precise excision of insertion elements and bacteriophage Mu growth.

We have used a papillation screening technique to isolate mutations that increase the precise excision of insertion elements. The three mutations isolated stimulated precise excision of Tn5, Tn10, and the IS elements. They had a large, 20- to 600-fold, effect on excision of Tn5 at various chromosomal sites. The varied stimulation for different Tn5 insertions showed that the mutations altered the relationship between a precise excision activity and the chromosomal sequence flanking an inserted Tn5. A much smaller stimulation was observed for insertions on the plasmid F'128. The stimulation was recA independent. The mutations also reduced the rate of production of bacteriophage Mu progeny. The mutations were mapped by two- and three-factor crosses with closely linked Tn10 insertions. They defined the uup locus, located at 21.3 min on the Escherichia coli map, next to pyrD.

Bacteriophage mu↗
PubMed1983

New concepts in medical bacteriology.

Traditional tests employed in a clinical microbiology laboratory for speciation of bacteria rely upon the presence of one or more gene products (biochemical profile) from a population of bacterial cells. These traits have been stable over a relatively long period of time, and the techniques have served us well. Current technology allows for modification and potential improvement of this system. By chemically separating DNA strands and employing recombinant DNA techniques, direct identification of bacteria becomes possible. These methods can be adapted directly to the clinical setting. In addition, specific gene products yield clinical disease; monoclonal antibodies directed against these products may speciate a bacterium indirectly through a unique gene product. Specific gene products also provide markers for epidemiologic investigation. All these technologies should find frequent clinical application in the next several years. The discoveries a century ago that germs cause infection and that different germs cause different infections prompted the development of a system of taxonomy for pathogenic microbes. It then became apparent that the identity of the germ infecting a patient could tell us more about his or her diagnosis and prognosis than could all of the clinical skills accumulated up to that time.

Anti-Bacterial Agents↗
PubMed1982

Molecular epidemiology of antibiotic resistance in salmonella from animals and human beings in the United States.

We collected serotyped isolates of salmonella from reference laboratories in the United States, tested their susceptibility to antibiotics, and extracted plasmids from isolates that were resistant to a different combination of antibiotics from each of three serotypes. Restriction-endonuclease digestion showed that within each of the three groups, plasmid molecules from animal and human isolates were often identical or nearly identical. One serotype-plasmid combination appeared to be endemic in cattle in 20 states and infected 26 persons in two states. The human cases, which were not recognizably related except for their common plasmids, appeared to be clustered in time but geographically dispersed, like cases in previous outbreaks spread by food products. These findings suggest that resistance plasmids may be extensively shared between animal and human bacteria, and that spread of multiresistant strains of salmonella among animals and human beings, as observed in Britain, may have been undetected in the United States for lack of comparable surveillance.

Animals↗
PubMed1980

Recombination genes on the Escherichia coli sex factor specific for transposable elements.

The Escherichia coli sex factor stimulates precise excision of transposons Tn5 and Tn10 from sites either within the bacterial chromosome or within the factor itself. We have isolated two kinds of mutations that affect this activity. The ferA mutations eliminate the stimulation; the ferB mutations enhance it in the presence of FerA+. We conclude that ferA defines a sex factor gene that stimulates precise excision. The ferB mutations also specifically increase the rate of recombination between two IS3 elements on F' lac-pro (F'128) in a reaction that requires the product of recA. The stimulation of this recombination by ferB also requires an active ferA gene, which implies that the ferA gene stimulates this reaction as well as precise excision. A ferA mutation was mapped at 84.2 kilobases on the F factor, and a ferB mutation was mapped at 82.5 kilobases. The fer mutants were obtained by an approach that permits the isolation of mutants affecting precise excision.

Chromosome Mapping↗