In addition to its prominence in producing genetic diversity in bacterial 
species, homologous recombination (HR) plays a key role in DNA repair and damage 
tolerance. The frequency of HR depends on several factors, including the 
efficiency of DNA repair systems as HR is involved in recovery of replication 
forks perturbed by DNA damage. Nucleotide excision repair (NER) is one of the 
major DNA repair pathways involved in repair of a broad range of DNA lesions 
generally induced by exogenous chemicals or UV-irradiation and its functions in 
the cells not exposed to DNA-damaging agents have attracted less attention. In 
this study we have developed an assay that enables to investigate HR between 
chromosomal loci of the soil bacterium Pseudomonas putida both in growing and 
stationary-phase cells. The present assay detects HR events between two 
non-functional alleles of phenol degrading genes that produce a functional 
allele and allow the growth of bacteria on phenol as a sole carbon source. Our 
results indicate that HR between chromosomal loci takes place mainly in the 
growing cells and the frequency of HR is reduced during the following starvation 
in NER-proficient P. putida but not in the case when bacteria lack UvrA or UvrB 
enzymes. The absence of UvrA or UvrB resulted in a hyper-recombination phenotype 
in P. putida, the cells were filamented and their growth was impaired even in 
the absence of exogenous DNA damage. However, NER-deficient derivatives that 
overcame growth defects emerged rapidly. Such adaptation resulted in the decline 
of the frequency of HR. Although HR in actively replicating P. putida was still 
elevated in the adapted variants of the UvrA- and UvrB-deficient strains, the 
dynamics of emergence of the recombinants in these strains turned similar to 
NER-proficient bacteria. Additionally, we observed that HR was enhanced in the 
absence of the transcription repair coupling factor Mfd in growing cells but not 
during starvation. The frequency of HR was not affected by the UvrA homologue 
UvrA2 neither in NER-proficient bacteria nor in the absence of UvrA, suggesting 
a minor role of UvrA2 in NER. Thus, we conclude that NER functions are important 
also without exogenously induced DNA damage in P. putida and both 
transcription-coupled and global genome NER act to suppress HR in growing cells, 
whereas UvrA and UvrB are involved in the maintenance of the genome integrity 
also in stationary-phase cells.