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 recBET-37 allele carrying multiple missense mutations. Phenotypic analysis has been performed with congenic menigococcal strains harboring either the wild-type recB allele or the recBET-37 allele. Congenic recBET-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 recBET-37, allele was able to complement the Escherichia coli recB21 mutation to UV resistance and proficiency in recombination. recBET-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 recBET-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 recBET- 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.
Phenotypes of naturally defective recb allele in Neisseria meningitidis clinical isolates
Del Giudice L;
2002
Abstract
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 recBET-37 allele carrying multiple missense mutations. Phenotypic analysis has been performed with congenic menigococcal strains harboring either the wild-type recB allele or the recBET-37 allele. Congenic recBET-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 recBET-37, allele was able to complement the Escherichia coli recB21 mutation to UV resistance and proficiency in recombination. recBET-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 recBET-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 recBET- 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.