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V Krishnapillai

Publications and source records attributed to V Krishnapillai.

53 records · Page 3Linked to original sources
PubMed1977

Expression of Klebsiella nif and his genes in Salmonella typhimurium.

Derivatives of Salmonella typhimurium carrying F prime or P prime plasmids with Klebsiella nif and his genes had specific nitrogenase activities similar to Klebsiella in selective conditions, even to showing "hyperinduction" under argon. No evidence was obtained for catabolite repression of normal nif expression but dibutyl cyclic AMP often augmented "hyperinduction". In non-selective conditions the Klebsiella his nif determinants were rapidly lost from the plasmids; the low levels of nif expression and temperature-sensitive his expression previously reported were probably due to ready loss of his nif in the test conditions used.

Cyclic AMP↗
PubMed1977

Characterization of Pseudomonas aeruginosa derepressed R-plasmids.

A genetic study of conjugal transmissibility of two R-plasmids was undertaken in Pseudomonas aeruginosa. Conjugally derepressed mutants of the R-plasmids were isolated, and examination of 11 independent mutants revealed that 10 were recessive to the wild-type transfer repressor, whereas 1 mutant was cis dominant. Cross-repression was observed between the two R-plasmids, suggesting that they have functionally equivalent systems for regulating the expression of tra loci. The derepressed R-plasmid mutants exhibited several characteristics, in addition to derepressed transfer, that were not expressed by the parental plasmids. These included sensitivity to certain donor-specific phages, inhibition of multiplication of a transducing phage, and, in the one case examined, a high degree of entry exclusion. The coexpression of these different functions suggests that their respective genetic loci are controlled by the same regulatory system as that of tra, or else that they are part of the tra complex.

Bacteriophages↗
PubMed1975

Mutations in Salmonella typhimurium conferring resistance to Felix O phage without loss of smooth character.

Several mutants obtained from smooth Salmonella typhimurium strains by selection for resistance to Felix O (FO) phage [whose receptor site includes the N-acetylglucosamine branch of the lipopolysaccharide (LPS) core] were smooth in cultural properties, antigenic character and phage sensitivity pattern (except for their FO resistance). However, the affected genes of several such 'FOR' (FO-resistant) mutants were shown by transduction of map in the short cysE-pyrE segment, which includes nearly all known rfa genes responsible for synthesis of LPS core. All of seven FOR mutants differed from their parents, and resembled rfa mutants with defects in the deeper part of the LPS core, by increased sensitivity to various antibiotics. One FOR mutant was non-virulent (LD50 greater than 10-7, compared with smaller than 100 for its parent); LT7 derivatives given this FOR gene by co-transduction with cysE+ were likewise non-virulent. It is inferred that FOR mutations affect the assembly of the inner part of the LPS core, perhaps causing incomplete blocks in glycosyl transferase reactions.

Acetylglucosamine↗
PubMed1971

Uridinediphosphogalactose-4-epimerase deficiency in Salmonella typhimurium and its correction by plasmoid-borne galactose genes of Escherichia coli K-12: effects on mouse virulence, phagocytosis, and serum sensitivity.

The synthesis of smooth lipopolysaccharide (LPS) in relation to mouse virulence and resistance to serum bactericidal activity in vitro and to rapid intravenous clearance in vivo was studied in Salmonella typhimurium by using a virulent [median lethal dose (LD(50)) = 10(2)], smooth, and genetically marked strain, a uridinediphosphogalactose epimerase-deficient mutant of it which was, therefore, rough, and a derivative of the mutant made smooth again by acquisition of the galactose-positive genes of Escherichia coli. The mutant was of reduced virulence (LD(50) = 10(6)) but the smooth derivative regained the virulence character typical of the parent. The non-smooth phenotype also made the mutant, but not the smooth relatives (parent and derivative), susceptible to serum bactericidal activity and also to rapid intravenous clearance by phagocytosis by the liver. The mutant was similarly treated by germ-free mice (expected to be relatively free of opsonizing antibodies). The clearance of the mutant could be impaired by prior intravenous inoculation of homologous bacteria or their LPS but was reversible by preopsonization of the second inoculum with nonimmune mouse serum, suggesting that the initial inoculum preempted the opsonizing antibodies. Independent evidence of clearance specificity was also provided in mixed inoculum experiments on impaired mice by the rapid clearance of an antigenically unrelated heptose-deficient mutant while maintaining the decelerated clearance of the epimerase mutant. The latter, however, was converted to accelerated clearance by the intravenous inoculation during the impaired state of anti-epimerase mutant immune mouse serum.

Animals↗
PubMed1971

Properties of a Salmonella typhimurium mutant with an incomplete deficiency of uridinediphosphogalactose-4-epimerase.

A galactose-negative mutant, nonleaky in respect to fermentation and utilization, isolated from a smooth Salmonella typhimurium strain by phage selection and inferred deficient of uridine diphosphate (UDP)-galactose-epimerase, was used for experiments on relation of somatic lipopolysaccharide (LPS) character to virulence. Extracts of induced mutant cells retained ca. 1% of wild-type epimerase activity and had only ca. 5% of wild-type kinase and uridyl transferase activities; also, some cultural properties of the mutant differed from those of mutants with complete defects of epimerase only. The mutant was not galactose sensitive, presumably because of its kinase defect. Although the mutant had the phage pattern (including C21-sensitivity) of an epimerase mutant, it was susceptible to transduction by phage P22 and was O-agglutinable, even when grown on defined medium; its LPS must therefore contain some O polymer, including endogenous galactose, resulting from residual epimerase activity. Growth on galactose-supplemented medium restored smooth phage sensitivity; since the mutant was partly inducible this may result, at least in part, from increased endogenous production of UDP-galactose. The mutant was made galactose positive by introduction of an F'-gal(+) plasmid. Base-change and frame-shift mutagens did not increase the frequency of reversion above the spontaneous rate. An insertion into the operator-promoter region of the gal operon seems the most likely mechanism of the mutation.

Adenine↗
PubMed1969

Salmonella abony-Salmonella typhimurium recombinant nonvirulent for the mouse.

A previous genetic investigation involving a mouse-nonvirulent Salmonella abony donor (high frequency of recombination) and a virulent S. typhimurium recipient indicated that two unlinked "low-virulence" loci determined nonvirulence. A nonvirulent recombinant was analyzed to determine the basis for its nonvirulence. The recombinant was smooth (like the parental strains) and prototrophic. The doubling time in mouse serum of the recombinant and the S. abony parent (both streptomycin-resistant) was longer than that of the wild-type streptomycin-sensitive ancestor of the S. typhimurium recipient. The virulent recipient also grew poorly in serum. However, the nonvirulence of the recombinant was probably not due to its inheritance of the streptomycin-resistance allele from the donor, because other recombinants were streptomycin-resistant but still virulent. Unlike the nonvirulent S. abony (but like the S. typhimurium), the recombinant was insusceptible to rapid intravenous clearance in normal mice. It therefore appears that neither of the "low-virulence" loci determine diminished virulence by enhancing phagocytosis. Clearance of the recombinant was enhanced by opsonization with immune serum. Counts of viable bacteria in the blood, liver, and spleen of normal mice after intravenous challenge showed that the recombinant, like the S. abony donor, failed to proliferate in the tissues, whereas the virulent S. typhimurium did so markedly. It is concluded that the nonproliferation of the recombinant was determined by one or both of the "low-virulence" loci from the nonvirulent S. abony donor.

Animals↗
PubMedDate not supplied

Insertions of the transposon Tn1 into the Pseudomonas aeruginosa chromosome.

The transposon Tn1 has been translocated to the chromosome of Pseudomonas aeruginosa from plasmid R18, following hydroxylamine mutagenesis of the plasmid. Twelve insertions were mapped to six distinct sites distal to 55 min of the origin of chromosome transfer by the plasmid FP2. These map locations were confirmed by host chromosome mobilization tests mediated by plasmids R18 or R91-5, due to Tn1 homology between plasmid and host chromosome. All the Tn1 chromosomal inserts were retransposable to other plasmids (Sa, R931 and R38). The behavior of Tn1 in P. aeruginosa was very similar to its behavior in Escherichia coli with respect to regional specificity, orientation of insertion and in serving as regions of homology for host chromosome mobilization by plasmids. This last property has permitted the demonstration that Tn1 on R18 and R91-5 is in opposite orientation with respect to the origin of transfer (oriT) of the two plasmids.

Chromosome Mapping↗