Carcinogenesis, Vol 18, 681-686, Copyright © 1997 by Oxford University Press
C Cullinane, CA Weber, G Dianov and VA Bohr
It has recently been reported that the XPD (ERCC2) gene is an integral
component of the basal transcription factor TFIIH. We have studied the
direct role of this repair gene on the fine structure of DNA repair in
hamster cells. The gene and strand specific DNA repair of UV induced
pyrimidine dimers was determined in wild-type hamster cells, in hamster
cells harboring a mutation in the gene homologous to the XPD gene and in
mutant cells transfected with the human XPD gene. In the mutant cells,
strand specific repair was severely deficient. In the transfected cells,
preferential and strand specific gene repair were restored to wild-type
levels. The results of the current study clearly demonstrate a direct role
for the XPD gene product both in the preferential repair and bulk repair of
pyrimidine dimers as well as its high functional conservation between
rodent and human cells. An in vitro transcription assay was employed to
investigate whether RNA polymerase II mediated transcription was also
affected by the transfection with the XPD gene. No change in transcription
between the mutant and transfected cells was observed. This suggests that
the role of XPD in repair can be distinguished from its role in TFIIH
dependent transcription initiation. Different functional domains of XPD
appear to be necessary for repair versus transcription.
ARTICLES
Restoration of preferential and strand specific gene repair in group 2 Chinese hamster ovary mutants (UV5) by the XPD (ERCC2) gene
Laboratory of Molecular Genetics, National Institutes on Aging, Baltimore, MD 21224, USA.
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