Complementation of the oxidatively damaged DNA repair defect in Cockayne syndrome A and B cells by Escherichia coli formamidopyrimidine DNA glycosylase

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• 作者：Monica Ropolo ; Paolo Degan ; Mara Foresta ; Mariarosaria D'Errico ; Denise Lasigliè ; Eugenia Dogliotti ; Gianluigi Casartelli ; Simonetta Zupo ; Aless ; ro Poggi ; Guido Frosina
• 关键词：Cockayne syndrome ; Oxidatively damaged DNA ; Expression ; Formamidopyrimidine DNA glycosylase ; DNA base excision repair
• 刊名：Free Radical Biology and Medicine
• 出版年：2007
• 出版时间：15 June 2007
• 年：2007
• 卷：42
• 期：12
• 页码：1807-1817
• 全文大小：1086 K

文摘

Repair of the oxidized purine 8-oxo-7,8-dihydroguanine (8-oxoGua) is inefficient in cells belonging to the B complementation group of Cockayne syndrome (CS-B), a developmental and neurological disorder characterized by defective transcription-coupled repair. We show here that cells belonging to the A complementation group (CS-A) are also defective in repair of 8-oxoGua and we demonstrate that expression of the Escherichia coli formamidopyrimidine DNA glycosylase (FPG) completely corrects the repair deficiency in both CS-A and CS-B cells. Phenotypically, CS-A cells are normally sensitive to toxicity and micronuclei induced by the oxidizing agent potassium bromate. CS-B cells display sensitivity to elevated concentrations of potassium bromate but this is not compensated by FPG expression, suggesting toxicity of lesions that are not FPG substrates. The data indicate that 8-oxoGua is not a major toxic and clastogenic lesion in CS cells.