2012 年 34 巻 3 号 p. 101-106
We have already shown that the re-joining step of excision repair inhibits the formation of comet tails. In this study, we investigated how the formation of comet tails is supported by the incision step of excision repair. Three different human cells that are defective in nucleotide excision repair (NER), namely, XP3OSSV (derived from an XP group A patient), XPL3KA (derived from an XP group C patient), and CS2OSSV (derived from a Cockayne syndrome group A patient), and one NER wild-type human cell, TK6, were used. They were exposed to alkylating agents, bleomycin (BLM), or UVC, and then slides for the comet assay were prepared. Alkylating agents and BLM induced positive responses in the four studied cells. On the other hand, UVC induced positive responses in TK6, XPL3KA, and CS2OSSV cells, but not in XP3OSSV cells. UVC did not induce positive responses in XP3OSSV cells in the presence of DNA repair inhibitors (araC and hydroxyurea) or in their absence. Comet-positive response upon UVC irradiation was observed later in CS2OSSV than in TK6 and XPL3KA cells. It declined earlier in XPL3KA than in TK6 cells. On the basis of our results, the following features are suggested: 1. The incision step of NER is necessary to form comet tails. 2. If either TCR or GGR of NER acts, the comet tails can be formed.
