Killer cell immunoglobulin-like receptor (KIR) genes and their HLA-C ligands in a Ugandan population

Killer cell immunoglobulin-like receptor (KIR) genes are expressed by natural killer cells and encoded by a family of genes exhibiting considerable haplotypic and allelic variation. HLA-C molecules, the dominant ligands for KIR, are present in all individuals and are discriminated by two KIR epitopes, C1 and C2. We studied the frequencies of KIR genes and HLA-C1 and C2 groups in a large cohort (n?=?492) from Kampala, Uganda, East Africa and compared our findings with published data from other populations in sub-Saharan Africa (SSA) and several European populations. We find considerably more KIR diversity and weaker linkage disequilibrium in SSA compared to the European populations and describe several novel KIR genotypes. C1 and C2 frequencies were similar to other SSA populations with a higher frequency of the C2 epitope (54.9 %) compared to Europe (average 39.7 %). Analysis of this large cohort from Uganda in the context of other African populations reveals variations in KIR and HLA-C1 and C2 that are consistent with migrations within Africa and potential selection pressures on these genes. Our results will help understand how KIR/HLA-C interactions contribute to resistance to pathogens and reproductive success.     

Transposon Tn5 mutagenesis of Pseudomonas fluorescens to isolate mutants deficient in antibacterial activity

Abstract Pseudomonas fluorescens was subjected to insertion mutagenesis studies using the transposon Tn5-GM to generate mutants deficient in antibacterial activity minus mutants. The transposon located on the temperature-sensitive plasmid pCHR84 was conjugally transferred into the non-pathogenic pseudomonad using the triparental mating procedure. Random integration of Tn 5 -GM into the chromosome of P. fluorescens was achieved by heat ttreatment of the transformed cells at 42°C. Approximately 2% of transconjugants revealed an auxotrophic phenotype indicating efficient integration of the employed transposon into the chromosome of P. fluorescens . One transposon insertion mutant was obtained showing an antibacterial activity minus phenotype. This mutant (MM-7) was found to be defective in the production of an unidentified antibacterial compound against B. subtilis . These results introduce Tn 5 transposon mutagenesis as a new useful tool for the molecular analysis of P. fluorescens .     

Leakiness of genetic markers and susceptibility to post-plating mutagenesis inEscherichia coli

WhenEscherichia coli strain AB1157 is subjected to starvation for threonine or leucine on solid media, threonine-independent or leucine-independent colonies continue to emerge for several days after plating. This process is strongly streptomycin dependent. Under identical conditions arginine-independent colonies do not arise when arginine starvation is imposed. Since thethr1 andleuB6 alleles of AB1157 could be classified as ‘leaky’ while theargE3 allele cannot be so classified, there seems to be a correlation between leakiness of mutant genetic markers and post-plating mutagenesis which counters the effect of the mutations. Some of the threonine-independent variants acquired the ability to increase the leakiness of otherwise nonleaky markers such asargE3 and permit development of arginine independence in arecA-dependent,lexA-independent manner. I show that these variants harbour a mutation, tentatively namedadi (adaptation inducer), at around 72 min on the genetic map, and that theadi mutation increases the intrinsic leakiness of alacZ (ochre) mutation, perhaps by enhanced translational error. These observations are discussed in relation to the phenomenon of ‘adaptive’ mutagenesis, its possible mechanism, and its specificity.     

Nitrofurantoin-resistant mutants of Escherichia coli: isolation and mapping

Summary Mutants of Escherichia coli resistant to nitrofurantoin have been isolated. The mutations, designated nfnA and nfnB were introduced individually into a multiply auxotrophic E. coli F^– strain and mapped by conjugation and transduction. nfnA is located at 79.8 min and nfnB at 13.0 min on the E. coli chromosome.     

A new toxin isolated from Xanthomonas malvacearum which inhibits mitochondrial ATP--ADP translocase

The pathogenic effect of cotton blight disease is influenced by Xanthomonas malvacearum toxin. The toxin has been highly purified and the interaction between the toxin and the energy-generating system of mitochondria has been characterized. The results show that the toxin inhibits the ATP-ADP translocase system of the mitochondria.