Mechanism of DNA Lesion Homing and Recognition by the Uvr Nucleotide Excision Repair System  

作　　者：Seung-Joo Lee Rou-Jia Sung Gregory L.Verdine 

机构地区：[1]Department of Stem Cell and Regenerative Biology,Harvard University,Cambridge,MA 02138,USA [2]Department of Molecular and Cellular Biology,Harvard University,Cambridge,MA 02138,USA [3]Department of Chemistry and Chemical Biology,Harvard University,Cambridge,MA 02138,USA

出　　处：《Research》2019年第1期592-602,共11页研究（英文）

基　　金：This work was supported by the National Institutes of Health Grant CA100742 to Gregory L.Verdine;National Cancer Center Postdoctoral Fellowship to Seung-Joo Lee.

摘　　要：Nucleotide excision repair(NER)is an essential DNA repair system distinguished from other such systems by its extraordinary versatility.NER removes a wide variety of structurally dissimilar lesions having only their bulkiness in common.NER can also repair several less bulky nucleobase lesions,such as 8-oxoguanine.Tus,how a single DNA repair system distinguishes such a diverse array of structurally divergent lesions from undamaged DNA has been one of the great unsolved mysteries in the feld of genome maintenance.Here we employ a synthetic crystallography approach to obtain crystal structures of the pivotal NER enzyme UvrB in complex with duplex DNA,trapped at the stage of lesion-recognition.Tese structures coupled with biochemical studies suggest that UvrB integrates the ATPase-dependent helicase/translocase and lesion-recognition activities.Our work also conclusively establishes the identity of the lesion-containing strand and provides a compelling insight to how UvrB recognizes a diverse array of DNA lesions.

关 键 词：REMOVE REPAIR DUPLEX 

分 类 号：Q53[生物学—生物化学]