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Self‐Resistance to an Antitumor Antibiotic: A DNA Glycosylase Triggers the Base‐Excision Repair System in Yatakemycin Biosynthesis
Author(s) -
Xu Hui,
Huang Wei,
He QingLi,
Zhao ZhiXiong,
Zhang Feng,
Wang Renxiao,
Kang Jingwu,
Tang GongLi
Publication year - 2012
Publication title -
angewandte chemie international edition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.831
H-Index - 550
eISSN - 1521-3773
pISSN - 1433-7851
DOI - 10.1002/anie.201204109
Subject(s) - dna glycosylase , gene , mutagenesis , dna repair , biology , dna , base excision repair , gene cluster , bacteria , in vivo , biochemistry , genetics , mutation
Resistance is (not) futile : The yatakemycin biosynthetic gene cluster involves the ytkR2 gene, which encodes a protein with homology to a recently discovered bacterial DNA glycosylase. Genetic validation in vivo, biochemical assays, and in vitro mutagenesis studies revealed that YtkR2 confers resistance for the bacteria by specifically recognizing and cleaving the YTM‐modified base (see scheme).