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J. Biol. Chem., Vol. 276, Issue 49, 45772-45779, December 7, 2001
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From the Cockayne Syndrome (CS) is a human genetic
disorder with two complementation groups, CS-A and CS-B. The
CSB gene product is involved in transcription-coupled
repair of DNA damage but may participate in other pathways of DNA
metabolism. The present study investigated the role of different
conserved helicase motifs of CSB in base excision
repair. Stably transformed human cell lines with site-directed
CSB mutations in different motifs within its putative
helicase domain were established. We find that CSB null and
helicase motif V and VI mutants had greater sensitivity than wild type
cells to
The Cockayne Syndrome Group B Gene Product Is Involved in General
Genome Base Excision Repair of 8-Hydroxyguanine in DNA*
,,,¶,,,, and
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. Whole cell extracts from CSB null and motif V/VI mutants had lower activity of 8-hydroxyguanine incision
in DNA than wild type cells. Also, 8-hydroxyguanine accumulated more in
CSB null and motif VI mutant cells than in wild type cells after exposure to -radiation. We conclude that a deficiency in general genome base excision repair of selective modified DNA base(s)
might contribute to CS pathogenesis. Furthermore, whereas the
disruption of helicase motifs V or VI results in a CSB phenotype, mutations in other helicase motifs do not cause this effect. The biological functions of CSB in different DNA repair pathways may be
mediated by distinct functional motifs of the protein.
*
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.
To whom correspondence should be addressed: Laboratory of
Molecular Gerontology, NIA, National Institutes of Health, 5600 Nathan
Shock Dr., Baltimore, MD 21224. Tel.: 410-558-8223; Fax: 410-558-8157; E-mail: vbohr@nih.gov.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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