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Functional importance of the family 1 glucosyltransferase UGT72B1 in the metabolism of xenobiotics in Arabidopsis thaliana

Functional importance of the family 1 glucosyltransferase UGT72B1 in the metabolism of... The Arabidopsis type 1 UDP‐glucose‐dependent glucosyltransferase UGT72B1 is highly active in conjugating the persistent pollutants 3,4‐dichloroaniline (DCA) and 2,4,5‐trichlorophenol (TCP). To determine its importance in detoxifying xenobiotics in planta, mutant plants where the respective gene has been disrupted by T‐DNA insertion have been characterized. Extracts from the knockout ugt72B1 plants showed radically reduced conjugating activity towards DCA and TCP and the absence of immunodetectable UGT72B1 protein. In contrast, activities towards phenolic natural products were unaffected. When aseptic root cultures were fed [14C]‐DCA, compared with wild types, the ugt72B1 plants showed a reduced rate of uptake of the xenobiotic and very little metabolism to soluble DCA‐glucose or associated polar conjugates. Instead, the knockouts accumulated non‐extractable radioactive residues, most probably associated with lignification. When the feeding studies were carried out with [14C]‐TCP, rates and routes of metabolism were identical in the wild type and knockouts, with TCP‐glucoside a major product in both cases. Similar differential effects on the metabolism of DCA and TCP were obtained in whole plant studies with wild type and ugt72B1 mutants, demonstrating that while UGT72B1 had a central role in metabolizing chloroanilines in Arabidopsis, additional UGTs could compensate for the conjugation of TCP in the knockout. TCP was equally toxic to wild type and ugt72B1 plants, while surprisingly, the knockouts were less sensitive to DCA. From this it was concluded that the glucosylation of DCA may not be as effective in xenobiotic detoxification as bound‐residue formation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Plant Journal Wiley

Functional importance of the family 1 glucosyltransferase UGT72B1 in the metabolism of xenobiotics in Arabidopsis thaliana

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References (48)

Publisher
Wiley
Copyright
Copyright © 2005 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0960-7412
eISSN
1365-313X
DOI
10.1111/j.1365-313X.2005.02398.x
pmid
15860014
Publisher site
See Article on Publisher Site

Abstract

The Arabidopsis type 1 UDP‐glucose‐dependent glucosyltransferase UGT72B1 is highly active in conjugating the persistent pollutants 3,4‐dichloroaniline (DCA) and 2,4,5‐trichlorophenol (TCP). To determine its importance in detoxifying xenobiotics in planta, mutant plants where the respective gene has been disrupted by T‐DNA insertion have been characterized. Extracts from the knockout ugt72B1 plants showed radically reduced conjugating activity towards DCA and TCP and the absence of immunodetectable UGT72B1 protein. In contrast, activities towards phenolic natural products were unaffected. When aseptic root cultures were fed [14C]‐DCA, compared with wild types, the ugt72B1 plants showed a reduced rate of uptake of the xenobiotic and very little metabolism to soluble DCA‐glucose or associated polar conjugates. Instead, the knockouts accumulated non‐extractable radioactive residues, most probably associated with lignification. When the feeding studies were carried out with [14C]‐TCP, rates and routes of metabolism were identical in the wild type and knockouts, with TCP‐glucoside a major product in both cases. Similar differential effects on the metabolism of DCA and TCP were obtained in whole plant studies with wild type and ugt72B1 mutants, demonstrating that while UGT72B1 had a central role in metabolizing chloroanilines in Arabidopsis, additional UGTs could compensate for the conjugation of TCP in the knockout. TCP was equally toxic to wild type and ugt72B1 plants, while surprisingly, the knockouts were less sensitive to DCA. From this it was concluded that the glucosylation of DCA may not be as effective in xenobiotic detoxification as bound‐residue formation.

Journal

The Plant Journal – Wiley

Published: May 1, 2005

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