7,8-Dihydro-8-oxoguanine (8-oxoG) is the most frequent mutagenic lesion caused 
by oxidative stress. Eukaryotic cells use a specific DNA glycosylase, OGG1, to 
excise 8-oxoG from DNA. The mild phenotype of OGG1 null mice has been attributed 
to the existence of alternative pathways, including Cockayne syndrome B 
(CSB)-dependent transcription coupled repair (TCR), for removal of 8-oxoG. We 
have studied repair and transcription activities at 8-oxoG lesions with a 
reconstituted transcription system (RTS; RNA polymerase II, TBP, TFIIA, TFIIB, 
TFIIE, TFIIF and TFIIH), as well as in cellular extracts and in vivo. All 
measurable repair activity at 8-oxoG lesions takes place in the 3'-direction 
from the lesion, indicating base excision repair (BER) activity and negligible 
role of nucleotide excision repair (NER). Although 8-oxoG has been shown to be 
preferentially removed from the transcribed strand, in vitro experiments with 
purified transcription factors failed to identify a definite block for RNA 
polymerase II at the lesion. However, a weak block was observed at the lesion 
during transcription carried out with RTS as well as with cellular extracts. RNA 
polymerase II was identified at the site of the lesion on obstructed templates. 
Wild-type cells, as well as cells carrying targeted mutations of genes required 
for removal of 8-oxoG, were transfected with a luciferase expression vector 
containing an 8-oxoG lesion. No significant obstruction at 8-oxoG lesions was 
observed by this in vivo approach. In control experiments transcription 
elongation was completely blocked by cisplatin.