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Pest Management Science 2019-Oct

Resistance to clethodim in Italian ryegrass (Lolium perenne ssp. multiflorum) from Mississippi and North Carolina.

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Vijay Nandula
Darci Giacomini
Benjamin Lawrence
William Molin
Jason Bond

Słowa kluczowe

Abstrakcyjny

Clethodim, an acetyl-CoA carboxylase (ACCase)-inhibiting herbicide, is one of the few postemergence chemical control options available to growers of Mississippi to manage glyphosate and/or other herbicide resistant Italian ryegrass populations. Recently, clethodim failed to adequately control Italian ryegrass populations across Mississippi. A sethoxydim, also an ACCase inhibitor, -resistant Italian ryegrass population from North Carolina was cross-resistant to clethodim. This research characterized the magnitude and mechanisms of clethodim resistance in the Mississippi and North Carolina Italian ryegrass populations via whole-plant herbicide dose response, cross resistance, and metabolism studies, and molecular analysis.

RESULTS
Two clethodim-resistant biotypes from Mississippi, MS24 and MS37, were 10- and 4-fold resistant, respectively, relative to a susceptible (SUS1) biotype. A North Carolina biotype, NC21, was 40-fold resistant to clethodim compared to SUS1. Two additional biotypes from North Carolina, NC22 and NC 23, recorded shoot dry weight reduction of only 17 to 30% of nontreated at the highest clethodim dose of 2.17 kg ha-1 , (8X). The NC22 biotype was cross-resistant to sethoxydim, fluazifop, quizalofop, and pinoxaden. Metabolic inhibitors such as piperonyl butoxide and 4-chloro-7-nitrobenzofurazan did not affect resistance of MS37, MS51, and NC22 biotypes to fenoxaprop, clethodim, or pinoxaden. The MS37 biotype had three target site mutations, I2041N, C2088R, and G2096A. Another clethodim-resistant biotype from Mississippi, MS51, had only the C2088R substitution. The NC22 and NC23 biotypes had I1781L, I2041N, and D2078G replacements.

This study shows that the mechanism of resistance to clethodim in Italian ryegrass from Mississippi and North Carolina is due to target site modifications in the ACCase gene leading to broad cross-resistance to other ACCase-inhibiting herbicides. This article is protected by copyright. All rights reserved.

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