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J. Biol. Chem., Vol. 277, Issue 34, 30832-30837, August 23, 2002
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From the Cockayne syndrome (CS) is a human disease
characterized by sensitivity to sunlight, severe neurological
abnormalities, and accelerated aging. CS has two complementation
groups, CS-A and CS-B. The CSB gene encodes the CSB protein
with 1493 amino acids. We previously reported that the CSB protein is
involved in cellular repair of 8-hydroxyguanine, an abundant lesion in
oxidatively damaged DNA and that the putative helicase motif V/VI of
the CSB may play a role in this process. The present study investigated the role of the CSB protein in cellular repair of 8-hydroxyadenine (8-OH-Ade), another abundant lesion in oxidatively damaged DNA. Extracts of CS-B-null cells and mutant cells with site-directed mutation in the motif VI of the putative helicase domain incised 8-hydroxyadenine in vitro less efficiently than wild type
cells. Furthermore, CS-B-null and motif VI mutant cells accumulated
more 8-hydroxyadenine in their genomic DNA than wild type cells after exposure to
The Cockayne Syndrome Group B Gene Product Is Involved in
Cellular Repair of 8-Hydroxyadenine in DNA*
,¶
Laboratory of Molecular Gerontology, NIA,
National Institutes of Health, Baltimore, Maryland 21224 and the
§ Chemical Science and Technology Laboratory, National
Institute of Standards and Technology, Gaithersburg, Maryland
20899-8311
-radiation at doses of 2 or 5 Gy. These results
suggest that the CSB protein contributes to cellular repair of 8-OH-Ade and that the motif VI of the putative helicase domain of CSB is required for this activity.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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