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Infection and Immunity, August 2002, p. 4185-4195, Vol. 70, No. 8
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.8.4185-4195.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Phenotypes of a Naturally Defective recB Allele in Neisseria meningitidis Clinical Isolates

Paola Salvatore,1,2 Cecilia Bucci,1,3 Caterina Pagliarulo,1 Maurizio Tredici,3 Roberta Colicchio,1 Giuseppina Cantalupo,1 Marcellino Bardaro,1 Luigi Del Giudice,4 Domenica R. Massardo,4 Alfredo Lavitola,1 Carmelo B. Bruni,1* and Pietro Alifano3*

Dipartimento di Biologia e Patologia Cellulare e Molecolare "L. Califano," Università di Napoli "Federico II," and Centro di Endocrinologia ed Oncologia Sperimentale "G. Salvatore," Consiglio Nazionale delle Ricerche, 80131 Naples,1 Dipartimento di Scienze Ambientali, Seconda Università di Napoli, 81100 Caserta,2 Dipartimento di Scienze e Tecnologie Biologiche e Ambientali, Università degli Studi di Lecce, 73100 Lecce,3 Istituto Internazionale di Genetica e Biofisica, Consiglio Nazionale delle Ricerche, 80125 Naples, Italy4

Received 21 February 2002/ Returned for modification 5 April 2002/ Accepted 17 May 2002

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 meningococcal 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.

* Corresponding author. Mailing address: Dipartimento di Biologia e Patologia Cellulare e Molecolare L. Califano," Università di Napoli "Federico II," Via S. Pansini 5, 80131 Naples, Italy. Phone: (39) 081 7462047. Fax: (39) 081 7703285. E-mail: brucar{at}unina.it.

* Corresponding author. Mailing address: Dipartimento di Scienze e Tecnologie Biologiche e Ambientali, Università degli Studi di Lecce, 73100 Lecce, Italy. Phone: (39) 0832 320856. Fax: (39) 0832 320626. E-mail: alifano{at}ilenic.unile.it.

Editor: J. T. Barbieri

Infection and Immunity, August 2002, p. 4185-4195, Vol. 70, No. 8
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.8.4185-4195.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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