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

Autor:	Lee SJ; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA., Sung RJ; Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA., Verdine GL; Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138, USA.; Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.; Department of Chemistry and Chemical Biology, Harvard University, Cambridge, MA 02138, USA.
Jazyk:	angličtina
Zdroj:	Research (Washington, D.C.) [Research (Wash D C)] 2019 Aug 28; Vol. 2019, pp. 5641746. Date of Electronic Publication: 2019 Aug 28 (Print Publication: 2019).
DOI:	10.34133/2019/5641746
Abstrakt:	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. Thus, 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 field 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. These 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. Competing Interests: The authors declare that they have no conflicts of interest with the contents of this article.
Databáze:	MEDLINE
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