Figure 4.

Hypothetical model of the role of the NER system in H. pylori.  DNA molecules enter the cytoplasm as ssDNAs. These highly recombinogenic substrates are loaded with RecA filaments which catalyze the invasion of chromosomal DNA whenever homology regions are found [37]. This invasion results in DNA distortions that are recognized by the UvrAB complex. Since UvrC does not seem to be essential for the strand incision, but is involved in the regulation of the import length, another endonuclease might be recruited to generate the incisions (X?). In homology to E. coli, UvrB might engage UvrD in order to remove the cut fragment and unwind the DNA. Finally, the nicked region will be repaired by DNA polymerase I and ligase using the donor DNA as template. Early in the process, UvrD competes for the RecA-ssDNA substrates and works as an anti-recombinase by dismantling the RecA filaments leading to strand restoration.