Organ-specific expression of glutathione S-transferases and the efficacy of herbicide safeners in Arabidopsis.
The functions of plant glutathione S-transferases (GSTs) under normal growth conditions are poorly understood, but their activity as detoxification enzymes has been harnessed in agriculture for selective weed control. Herbicide safeners protect monocot crops from herbicide injury but have little effect on weedy monocot or dicot species. Protection by safeners is associated with expression of herbicide-metabolizing enzymes including GSTs, but the basis for selective action of safeners between monocots and dicots is not known. To address this question we have studied the response of Arabidopsis (Arabidopsis thaliana) to various safeners. Benoxacor, fenclorim, and fluxofenim did not protect Arabidopsis from herbicide injury but did induce RNA expression of the glutathione-conjugate transporters encoded by AtMRP1, AtMRP2, AtMRP3, and AtMRP4. These safeners also induced the organ-specific expression of AtGSTU19 and AtGSTF2, two previously characterized Arabidopsis GSTs from different classes of this enzyme family. RNA hybridization, immunoblot, and reporter gene analyses indicated expression of AtGSTU19 induced by safeners predominated in roots. To test the hypothesis that increased expression of AtGSTU19 would be sufficient to provide tolerance to chloroacetamide herbicides, a chimeric gene was produced containing the open reading frame for this GST driven by a constitutive promoter. Plants containing this transgene had a modest increase in AtGSTU19 protein, predominantly in roots, but this had no effect on tolerance to chloroacetamide herbicides. The localized induction of GSTs by safeners in roots of Arabidopsis may explain why these compounds are unable to provide herbicide tolerance to dicot plant species.
DeRidder
Ben P
BP
Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, Indiana 47907, USA.
Goldsbrough
Peter B
PB
D000081:Acetamides / Q000037:antagonists & inhibitors / Q000633:toxicity; D000098:Acetophenones / Q000494:pharmacology; D017360:Arabidopsis / Q000187:drug effects / Q000201:enzymology* / Q000235:genetics; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism*; D018506:Gene Expression Regulation, Plant; D017930:Genes, Reporter; D005982:Glutathione Transferase / Q000235:genetics / Q000378:metabolism*; D006540:Herbicides / Q000037:antagonists & inhibitors* / Q000633:toxicity; D026901:Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism; D010078:Oxazines / Q000494:pharmacology; D010091:Oximes / Q000494:pharmacology; D018517:Plant Roots / Q000235:genetics / Q000378:metabolism; D030821:Plants, Genetically Modified / Q000033:anatomy & histology / Q000187:drug effects / Q000201:enzymology; D011743:Pyrimidines / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D014018:Tissue Distribution; D019076:Transgenes
D000081:Acetamides; D000098:Acetophenones; D029681:Arabidopsis Proteins; D006540:Herbicides; D026901:Membrane Transport Proteins; D010078:Oxazines; D010091:Oximes; D011743:Pyrimidines; D012333:RNA, Messenger; D011993:Recombinant Fusion Proteins; C501523:fenclorim; C078188:2-chloro-N-(ethoxymethyl)-N-(2-methyl-6-(trifluoromethyl)phenyl)acetamide; C108005:fluxofenim; C478066:GSTF2 protein, Arabidopsis; C472235:GSTU19 protein, Arabidopsis; D005982:Glutathione Transferase; C085163:benoxacor