SummaryMeningococcal gdhA , encoding the NADP-specific Lglutamate dehydrogenase (NADP-GDH), is essential for systemic infection in an infant rat model. In this paper, a limited transcriptional analysis detected differences in gdhA expression among clinical isolates. In strains expressing high levels of gdhA mRNA, two promoters, gdhA P1 and gdhA P2, initiated transcription of gdhA . In contrast, in strains expressing low mRNA levels, gdhA P2 was not active because of weak expression of gdhR , an associated regulatory gene. Gene knock-out and complementation of a gdhR -defective mutant confirmed that GdhR is a positive regulator for gdhA P2. Trans -activation of gdhA P2 was maximal in complex medium during late logarithmic growth phase and in chemical defined medium (MCDA) when glucose (MCDA-glucose) instead of lactate (MCDA-lactate) was used as a carbon source in the presence of glutamate. gdhR knockout mutants lost both growth phase and carbon source regulation, and exhibited a growth defect more severe in MCDA-glucose than in MCDA-lactate. DNAprotein interaction studies demonstrated that 2-oxoglutarate, a product of the catabolic reaction of the NADP-GDH and an intermediate of the tricarboxylic acid (TCA) cycle, inhibits binding of GdhR to gdhA P2.
We show that, in particular experimental conditions, the time course of the radiant fluxes, measured from a bioluminescent emission of a Vibrio harveyi related strain, collapse after suitable rescaling onto the Gumbel distribution of extreme value theory. We argue that the activation times of the strain luminous emission follow the universal behavior described by this statistical law, in spite of the fact that no extremal process is known to occur.
Neisseria meningitidis strains belonging to the hypervirulent lineage ET-37 and several unrelated strains are extremely UV sensitive. The phenotype is consequent to the presence of a nonfunctional recB ET-37 allele carrying multiple missense mutations. Phenotypic analysis has been performed with congenic meningococcal strains harboring either the wild-type recB allele or the recB ET-37 allele. Congenic recB ET-37 meningococci, in addition to being sensitive to UV, were defective both in repair of DNA lesions induced by UV treatment and, partially, in recombination-mediated transformation. Consistently, the wild-type, but not the recB ET-37 , allele was able to complement the Escherichia coli recB21 mutation to UV resistance and proficiency in recombination. recB ET-37 meningococci did not exhibit higher frequencies of spontaneous mutation to rifampin resistance than recB-proficient strains. However, mutation rates were enhanced following UV treatment, a phenomenon not observed in the recB-proficient counterpart. Interestingly, the results of PCR-based assays demonstrated that the presence of the recB ET-37 allele considerably increased the frequency of recombination at the pilin loci. The main conclusion that can be drawn is that the presence of the defective recB ET-37 allele in N. meningitidis isolates causes an increase in genetic diversity, due to an ineffective RecBCD-dependent DNA repair and recombination pathway, and an increase in pilin antigenic variation.
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