Nucleic Acids Research, Vol 27, Issue 5 1365-1368, Copyright © 1999 by Oxford University Press
G Dianov, C Bischoff, M Sunesen and VA Bohr
The incision of the 8-oxoguanine in DNA by normal and Cockayne Syndrome
(CS) cell extracts has been investigated. The incision in extracts derived
from CS cells was approximately 50% of the incision level compared with
extracts prepared from normal cells. In contrast, the incision rate of
uracil and thymine glycol was not defective in CS cells. The deficiency in
8-oxoguanine incision was also demonstrated in a CS family. Whereas the
proband had markedly less incision compared with the normal siblings, the
parents had intermediate levels. The low level of 8-oxoguanine-DNA
glycosylase in CS extracts correlates with the reduced expression of the
8-oxoguanine-DNA glycosylase gene (hOGG1) in CS cells. Both the levels of
expression of the hOGG1 gene and the incision of 8-oxoguanine in
DNAincreased markedly after transfection of CS-B cells with the CSB gene.
We suggest that the CSB mutation leads to deficient transcription of the
hOGG1 gene and thus to deficient repair of 8-oxoguanine in DNA.
ARTICLES
Repair of 8-oxoguanine in DNA is deficient in Cockayne syndrome group B cells
Laboratory of Molecular Genetics, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.
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