Resistance to protoporphyrinogen oxidase inhibitor herbicides in giant ragweed ( Ambrosia trifida ) is associated with a novel R98Q target-site mutation in PPO2
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BACKGROUND
Reduced control of giant ragweed ( Ambrosia trifida L.) with protoporphyrinogen oxidase (PPO)-inhibiting herbicides was recently reported in two southern Illinois populations, VRC and TMS. The objectives of this study were to assess resistance to postemergence-applied PPO inhibitors in VRC and TMS, evaluate VRC response to acetolactate synthase (ALS)- and enolpyruvyl shikimate phosphate synthase (EPSPS)-inhibiting herbicides, and identify target-site mechanisms associated with PPO-inhibitor resistance.
RESULTS
Based on LD estimates, VRC resistance ratios ranged from 1.1- to 3.7-fold for lactofen and 2.2- to 6.9-fold for fomesafen relative to PPO-sensitive populations SIU and DSO. In TMS, LD estimates were 257.4 g ai ha ¹ for lactofen and 318.4 g ai ha ¹ for fomesafen. Glyphosate LD estimates exceeded three times the labeled field rate in VRC, SIU, and DSO, whereas VRC and SIU had higher cloransulam-methyl LD estimates than DSO. Whole-transcriptome sequencing identified polymorphisms in PPX1 and PPX2 ; however, only PPO2 R98Q altered a catalytic-domain binding-pocket residue and was considered likely to contribute to resistance in VRC. R98Q was absent in TMS, and PPX1 and PPX2 expression did not differ among populations.
CONCLUSION
VRC and TMS have evolved resistance to lactofen and fomesafen, and VRC also exhibited reduced sensitivity to cloransulam-methyl and glyphosate. PPO2 R98Q is novel in A. trifida and, to our knowledge, represents the first report of this mutation associated with PPO-inhibitor resistance in plants. The absence of target-site alterations in TMS suggests a potential non-target-site basis for resistance. These findings highlight the need for integrated, diversified management to further reduce herbicide selection pressure.
