Abstract

ABSTRACTImidazolinone‐resistant (IR) wheat (Triticum aestivum L.) was released for commercial production in portions of the USA in 2002 and has provided growers with a new technology to selectively control winter annual grass weeds. Imidazolinone herbicides inhibit acetolactate synthase (ALS) in susceptible plants; however, IR wheat has an altered target site which confers resistance to these herbicides. The mutation‐derived resistance trait of most commercially available IR winter wheat cultivars is located on the D‐genome; however, winter and spring wheat cultivars with the resistance trait on the A, B, or D genome or on multiple genomes are currently under development. Four groups of near‐isoline wheat with spring or winter growth habit and resistance genes on the B, D, or both B and D genomes were compared for whole plant and ALS enzyme response to imazamox. Biomass accumulation after treatment was similar among B‐ and D‐ genome resistant winter wheat biotypes and was always higher than B‐ and D‐genome resistant spring wheat biotypes. D‐genome resistant spring wheat was more resistant than B‐genome resistant spring wheat and the two‐gene resistant spring wheat had an additive level of tolerance to imazamox compared with single‐gene resistant spring wheat. Growth habit (spring vs. winter) did not affect in vitro ALS activity among B‐ or among D‐genome resistant cultivars; however, D‐genome resistant cultivars had significantly higher in vitro ALS activity in the presence of imazamox compared with B‐genome resistant cultivars regardless of growth habit. D‐genome resistance appears to provide greater tolerance to imazamox compared with B‐genome resistance; however, multiple‐genome resistance likely will be required to consistently avoid crop injury in spring wheat from labeled U.S. rates. Although ALS extracted from winter wheat and spring wheat responded similarly to imazamox, whole plant responses demonstrates that tolerance is affected by factors other than resistance gene location.

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