Nucleotide excision repair (NER) is universally used to recognize and remove 
many types of DNA damage. In eubacteria, the NER system typically consists of 
UvrA, UvrB, UvrC, the UvrD helicase, DNA polymerase I, and ligase. In addition, 
when DNA damage blocks transcription, transcription-repair coupling factor 
(TRCF), the product of the mfd gene, recruits the Uvr complex to repair the 
damage. Previous work using selected mutants and assays have indicated that 
pathogenic Neisseria spp. carry a functional NER system. In order to 
comprehensively examine the role of NER in Neisseria gonorrhoeae DNA 
recombination and repair processes, the predicted NER genes (uvrA, uvrB, uvrC, 
uvrD, and mfd) were each disrupted by a transposon insertion, and the uvrB and 
uvrD mutants were complemented with a copy of each gene in an ectopic locus. 
Each uvr mutant strain was highly sensitive to UV irradiation and also showed 
sensitivity to hydrogen peroxide killing, confirming that all of the NER genes 
in N. gonorrhoeae are functional. The effect of RecA expression on UV survival 
was minor in uvr mutants but much larger in the mfd mutant. All of the NER 
mutants demonstrated wild-type levels of pilin antigenic variation and DNA 
transformation. However, the uvrD mutant exhibited higher frequencies of 
PilC-mediated pilus phase variation and spontaneous mutation, a finding 
consistent with a role for UvrD in mismatch repair. We conclude that NER 
functions are conserved in N. gonorrhoeae and are important for the DNA repair 
capabilities of this strict human pathogen.