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Biomedical subjects

J R Walker

Publications and source records attributed to J R Walker.

At least 181 records · Page 10Linked to original sources
PubMed1975

The effects of aeration on glucose catabolism in Penicillium expansum.

Polyacrylamide-disc gel electrophoresis and quantitative enzyme assays showed that the pathways of glucose catabolism and secondary metabolism in Penicillium expansum were dependent on the degree of aeration of the cultures. The isoenzyme patterns and specific activities of aldolase and succinate dehydrogenase indicated that glycolysis and the tricarboxylic acid cycle operated under conditions of both limited and efficient aeration (i.e. in cultures grown statically or on an orbital shaker). At high levels of aeration the growth rate was faster and synthesis of extracellular pectolytic enzymes was enhanced, whilst the activities of glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase showed that the pentose-phosphate shunt was important in glucose catabolism during the trophophase of growth. In contrast, under conditions of low aeration this latter pathway was virtually undetectable, growth was slower, pectolytic enzyme production low and large concentrations of secondary metabolites (6-methylsalicylic acid, patulin and citrinin) accumulated.

Aerobiosis↗
PubMed1975

Effects of a human plasma fraction on the release of chemotactic factors and anaphylatoxin from complement.

A fraction prepared from normal human plasma inhibits the release of chemotactic factors and anaphylatoxin when complement is activated by the alternate but not by the classical pathway. The fraction gave no interference with the actions of the released substances on either leucocytes or guinea-pig isolated ileum. The possible relation of this effect to the mechanism of the anti-inflammatory actions of the plasma fraction is discussed.

Anaphylaxis↗
PubMed1975

Effects of a human plasma fraction on leucocyte migration into inflammatory exudates.

A fraction prepared from normal human plasma inhibits the migration of polymorphonuclear and mononuclear leucocytes into inflammatory exudates produced by the intrapleural injection of carrageeman or turpentine by the subcutaneous implantation of polyvinyl sponges in the rat. The mechanism of the effect does not involve complement depletion.

Animals↗
PubMed1975

Regulation of bacterial cell division: temperature-sensitive mutants of Escherichia coli that are defective in septum formation.

Mutations ts2158 and ts1882, which confer temperature sensitivity of septum formation, map near leu in the region of min 2.0 to 2.1 on the Escherichia coli chromosome. These mutants stop division abruptly and grow as filaments at 42 C; when returned to 28 C, division resumes after about 30 min to produce short cells. The product of the gene defined by these mutations probably is required during all stages of septum formation rather than specifically for initiation of septation. Filaments that formed at 42 C contained incomplete constrictiions (septa). When actively dividing filaments (i.e., those incubated at 28 C until division resumed) were shifted to 42 C a second time, division again stopped abruptly and incomplete constrictions persisted during the incubation at 42 C. Filaments that were subjected to 28 C incubation for a brief time (10, 20, or 30 min) before being shifted again to 42 C did not resume division as would be expected of a strain defective in initiating septation. Mutations ts 1882 and ts2158 and recessive to the ts+ allele, which is consistent with the interpretation that these mutations cause the loss of a function. They did not complement each other and presumably represent one cistron. Mutants carrying ts1882 and ts2158 mutations were compared with a mutant defective in the ftA allele, also known to map near leu.

Cell Division↗
PubMed1975

Strain-specific difference that affects the inhibition of division of Escherichia coli filaments by chloramphenicol.

The Escherichia coli mutations ts1882 and ts2158 cause temperature-sensitive septum formation and result in growth of cells as long, multinucleate, nonseptate filaments at 42 C. When filaments are transferred to 28 C, they divide into short cells. Chloramphenicol, when added to cultures of filaments at the time of temperature reduction. Inhibited division of filaments when these temperature-sensitive mutations were present in the K-12 strain AB1157. However, when the ts1882 and ts2158 mutations were present in another k-12 strain, UTH4113, filaments of these strains divided in the presence of chloramphenicol.

Bacterial Proteins↗
PubMed1974

Regulation of bacterial cell division: genetic and phenotypic analysis of temperature-sensitive, multinucleate, filament-forming mutants of Escherichia.

Three mutants of Escherichia coli K-12 which form filaments during 42 C incubation have been characterized. The mutant strains AX621, AX629, and AX655 continued to grow and to synthesize deoxyribonucleic acid at 42 C for 150 to 180 min, after which time growth ceased. When cultures of the mutants were transferred from 42 to 28 C, septation of the filaments began after a 25- to 30-min period and continued at a greater than normal rate until no filaments remained. Addition of chloramphenicol at the time of transfer from 42 to 28 C prevented cell division in strain AX655 and caused lysis of strains AX621 and AX629. The temperature sensitivity mutation in each strain mapped near leu. For strain AX621, the mutation was specifically located between leu and nadC by P1 transduction. Properties of these strains are compared with those of other cell division mutants.

Azides↗
PubMed1974

Bacterial cell division regulation: characterization of the dnaH locus of Escherichia coli.

The dnaH locus is the fourth gene to be identified as required for deoxyribonucleic acid polymerization in Escherichia coli. A temperature-sensitive mutant defective in this gene exhibited an abrupt decrease in rate of deoxyribonucleic acid synthesis when shifted to 42 C. The locus mapped in the proC-purE region of the chromosome by conjugation and was co-transducible with purE. dnaH(+) is carried on the F'(13) episome and is dominant over the dnaH(-) mutation.

Cell Division↗
PubMed1973

Inhibition of lipid synthesis in Escherichia coli cells by the antibiotic cerulenin.

The antibiotic cerulenin markedly inhibits the growth of Escherichia coli. The effects of the antibiotic on cellular syntheses were studied by measuring the incorporation of labeled precursors into lipids and macromolecules. During the first 40 min after the addition of cerulenin to a culture of growing cells, lipid synthesis was inhibited more than 90% and ribonucleic acid and deoxyribonucleic acid synthesis about 25%, whereas protein synthesis was not affected. At later periods after cerulenin addition (1 to 2 h), the inhibition of cell growth and of lipid and protein synthesis was complete. Upon removal of cerulenin from the culture, growth was restored and lipid synthesis resumed more rapidly than did the synthesis of protein. Addition of both palmitate and oleate, but not of either fatty acid alone, reversed the inhibition of growth by cerulenin. These findings support the conclusion that the antibiotic effects of cerulenin are due to a specific inhibition of fatty acid synthesis.

Anti-Bacterial Agents↗
PubMed1973

Bacterial cell division regulation: lysogenization of conditional cell division lon - mutants of Escherichia coli by bacteriophage.

The lon(-) mutants of Escherichia coli grow apparently normally except that, after temporary periods of inhibition of deoxyribonucleic acid synthesis, septum formation is specifically inhibited. Under these conditions, long, multinucleate, nonseptate filaments result. The lon(-) mutation also creates a defect such that wild-type bacteriophage lambda fails to lysogenize lon(-) mutants efficiently and consequently forms clear plaques on a lon(-) host. Two lines of evidence suggest that this failure probably results from interference with expression of the lambdacI gene, which codes for repressor, or with repressor action:-(i) when a lon(-) mutant was infected with a lambdacII, cIII, or c Y mutant, there was an additive effect between the lon(-) mutation and the lambdac mutations upon reduction of lysogenization frequency; and (ii) lon(-) mutants permitted the growth of the lambdacro(-) mutant under conditions in which the repressor was active. The isolation of lambda mutants (lambdatp) which gained the ability to form turbid plaques on lon(-) cells is also reported.

Cell Division↗