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Journal of Bacteriology, September 2009, p. 5613-5621, Vol. 191, No. 18
0021-9193/09/$08.00+0     doi:10.1128/JB.00535-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Pilin Antigenic Variation Occurs Independently of the RecBCD Pathway in Neisseria gonorrhoeae{triangledown}

R. Allen Helm and H. Steven Seifert*

Northwestern University, Feinberg School of Medicine, Department of Microbiology-Immunology, Chicago, Illinois 60611

Received 21 June 2009/ Accepted 1 July 2009

Type IV pilus expression has been strongly implicated in the virulence of Neisseria gonorrhoeae, the causative agent of gonorrhea. In Neisseria, these pili undergo frequent antigenic variation (Av), which is presumed to allow reinfection of high-risk groups. Pilin Av is the result of RecA-mediated recombination events between the gene encoding the major pilin subunit (pilE) and multiple silent pilin locus (pilS) copies, utilizing a RecF-like recombination pathway. The role of RecBCD in pilin Av has been controversial. Previous studies measuring pilin Av in recB and recD mutants in two independent strains of N. gonorrhoeae (MS11 and FA1090) by indirect methods yielded conflicting results. In addition, these two laboratory strains have been suggested to express very different DNA repair capabilities. We show that the FA1090 and MS11 parental strains have similar abilities to repair DNA damage via UV-induced DNA damage, nalidixic acid-induced double-strand breaks, and methyl methanesulfonate-induced alkylation and that RecB and RecD are involved in the repair of these lesions. To test the role of the RecBCD pathway in pilin Av, the rate and frequency of pilin Av were directly measured by sequencing the pilE locus in randomly selected piliated progeny of both MS11 and FA1090 in recB and recD mutants. Our results definitively show that recB and recD mutants undergo pilin Av at rates similar to those of the parents in both strain backgrounds, demonstrating that efficient pilin Av is neither enhanced nor inhibited by the RecBCD complex.

* Corresponding author. Mailing address: Department of Microbiology-Immunology, Northwestern University, Feinberg School of Medicine, S213, 303 East Chicago Avenue, Chicago, IL 60611. Phone: (312) 503-9788. Fax: (312) 503-1339. E-mail: h-seifert{at}northwestern.edu

{triangledown} Published ahead of print on 10 July 2009.

Journal of Bacteriology, September 2009, p. 5613-5621, Vol. 191, No. 18
0021-9193/09/$08.00+0     doi:10.1128/JB.00535-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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