Nucleic Acids Research, 2010, Vol. 38, No. 17 5701 Figure 7. Excision assay for ssDNAs containing various kinds of damaged bases. The 50-end-labelled ssDNA containing a damaged base was reacted with 3-mM TTHB178 at 37 or 60 C. The respective substrates contained hypoxanthine (A), xanthine (B), uracil (C), 8-oxoguanine (D), a reduced abasic site (E), an abasic site (F), O4-methylthymine (G) and O6-methylguanine (H). In all the panels, ‘C’ means the substrate incubated at 60 C for 60 min without TTHB178. ‘M’ means the 16- (in A and B), 10- (in C, D, E, G and H) and 9-mer (in F) marker DNAs. The reaction time is shown at the top of the panels. (16,17). This model is in good agreement with our result that the recJ disruption did not aﬀect the sensitivity to H2O2. In addition, as shown in Supplementary Figure S4, tthb178 was actively transcribed especially in the late stationary phase. This result also implies the involvement of tthb178 in the repair, because cells in the late stationary phase are thought to be under serious oxidative stress, which can yield deaminated bases. Our in vivo experiments also indicate that RecJ but not Tth ExoI plays a signiﬁcant role in the repair of DNA damages caused by UV-C irradiation. UV-C irradiation mainly induces pyrimidine dimers, (6-4) photoproducts and DSBs (44). As pyrimidine dimers and (6-4) photo- products are repaired mainly by nucleotide excision repair (NER) (49), our results indicate the possible involvement of RecJ in NER. However, it is believed that ssExos do not play a critical role in the NER pathway (65). Instead, RecJ is suggested to be involved in the recovery of replication forks at blocking DNA lesions caused by UV irradiation (66). Our result also can be interpreted in the context of the rescue of arrested replication forks after UV-C irradiation. It should be mentioned that the double disruption of tthb178 and recJ caused the more severe sensitivity to UV-C irradiation than the single disruption of recJ. It can be speculated that Tth ExoI and RecJ participate in separate pathways for the repair of UV-induced damage, and the Tth ExoI-dependent pathway might be stimulated when the RecJ-dependent one is inactive.