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. 2006 Nov 16;25(23):5481–5491. doi: 10.1038/sj.emboj.7601403

Figure 1.

Figure 1

Bypass of oxidative lesions. (A) The transcription template contains a single oxoG-, Tg- or OHdU-lesion located 488/489 bp downstream of the AdMLP promoter start site. The oxidative lesion abolishes the ApaLI restriction site. (B) In vitro transcription of oxidative lesion containing template on the transcribed strand using either RTS (lanes 1–5), or HeLa NE (lanes 6–10) or on the non-transcribed strand (NTS) using RTS (lanes 11–13). Quantitative data (mean±s.d.) are derived from at least three independent experiments. Arrest (489 nt) and bypass (525 nt) transcripts are indicated. (C) Glycosylase assays (as described by Shimizu et al (2003) (lanes 1–3) and transcription assays (lanes 4–6) on an DNA-oxoG using RTS, HeLa and Ogg1−/− NE (kind gift of A Klungland). Quantitative transcription data (mean±s.d.) are derived from at least three independent experiments. (D) Repair of the damaged DNA templates as indicated at the top of the panel during the transcription reaction (lower panel). Templates (1464 bp), incubated in the presence of either RTS or HeLa NE, were next subjected to digestion by ApaLI. The presence of bands corresponding to 892 and 527 bp indicates digestion by ApaLI and thus repair of the lesion.