Journal
PEST MANAGEMENT SCIENCE
Volume 71, Issue 9, Pages 1274-1280Publisher
JOHN WILEY & SONS LTD
DOI: 10.1002/ps.3922
Keywords
ALS assay; herbicide resistance mechanism; ALS gene sequencing; Illumina HiSeq; yellow nutsedge; Cyperus esculentus
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Funding
- Arkansas Rice Promotion Board
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BACKGROUNDYellow nutsedge is one of the most problematic sedges in Arkansas rice, requiring the frequent use of halosulfuron (sulfonylurea) for its control. In the summer of 2012, halosulfuron at 53 g ha(-1) (labeled field rate) failed to control yellow nutsedge. The level of resistance to halosulfuron was determined in the putative resistant biotype, and its cross-resistance to other acetolactate synthase (ALS) inhibitors from four different herbicide families. ALS enzyme assays and analysis of the ALS gene were used to ascertain the resistance mechanism. RESULTSNone of the resistant plants was killed by halosulfuron at a dose of 13 568 g ha(-1) (256x the field dose), indicating a high level of resistance. Based on the whole-plant bioassay, the resistant biotype was not controlled by any of the ALS-inhibiting herbicides (imazamox, imazethapyr, penoxsulam, bispyribac, pyrithiobac-sodium, bensulfuron and halosulfuron) tested at the labeled field rate. The ALS enzyme from the resistant biotype was 2540 times less responsive to halosulfuron than the susceptible biotype, and a Trp(574)-to-Leu substitution was detected by ALS gene sequencing using the Illumina HiSeq. CONCLUSIONThe results suggest a target-site alteration as the mechanism of resistance in yellow nutsedge, which accounts for the cross-resistance to other ALS-inhibiting herbicide families. (c) 2014 Society of Chemical Industry
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