Illegitimate recombination is a major cause of genetic instability in 
prokaryotes as well as in eukaryotes. This recombination usually occurs at a low 
frequency, but it is greatly enhanced by UV irradiation or other environmental 
stresses. DNA damages produced by these environmental stresses are thought to 
induce DNA double-strand breaks, leading to illegitimate recombination. In this 
paper we show that UV-induced illegitimate recombination is enhanced by 
mutations of nucleotide excision repair genes, uvrA or uvrB, and partially by 
uvrC mutation, but not by uvrD mutation. Unexpectedly, the recombination was 
enhanced by the uvrA uvrB double mutation even without UV irradiation, but the 
uvrB uvrC double mutation has not shown this effect, suggesting that 
illegitimate recombination is mostly suppressed by UvrA and UvrB. Moreover, 
illegitimate recombination was synergistically enhanced by the recQ uvrA double 
mutation. In addition, overproduction of the UvrA protein suppressed the 
hyperrecombination phenotype of the recQ or uvrB mutant, but it did not affect 
the UV-sensitive phenotype of the uvrB mutant. We concluded that the UvrAB 
complex suppresses illegitimate recombination in a pathway shared with RecQ 
helicase. In addition, UvrA protein alone can suppress illegitimate 
recombination in the pathway, in which RecQ helicase and UvrAB complex work. 
Possible functions of the proteins involved in these pathways are also 
discussed.