Format

Send to

Choose Destination
Angew Chem Int Ed Engl. 2012 Oct 15;51(42):10532-6. doi: 10.1002/anie.201204109. Epub 2012 Sep 17.

Self-resistance to an antitumor antibiotic: a DNA glycosylase triggers the base-excision repair system in yatakemycin biosynthesis.

Author information

1
State Key Laboratory of Bioorganic and Natural Products Chemistry, Chinese Academy of Sciences, China.

Abstract

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).

PMID:
22987648
DOI:
10.1002/anie.201204109
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center