BACKGROUND: Yellow 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.
RESULTS: None of the resistant plants was killed by halosulfuron at a dose of 13 568 g ha−1 (256× 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 Trp574-to-Leu substitution was detected by ALS gene sequencing using the Illumina HiSeq.
CONCLUSION: The 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..