Abstract
AbstractThroughout eastern Arkansas, Palmer amaranth resistant to protoporphyrinogen oxidase (PPO)-inhibiting herbicides (Group 14 herbicides) has become widespread. Most PPO-resistant Palmer amaranth biotypes possess a target-site mutation, but a metabolic resistance mechanism to fomesafen (Group 14) has also been identified. Once metabolic resistance manifests, plants may also be tolerant to other herbicides and sites of action. To evaluate whether varying spray parameters affected control of PPO-resistant Palmer amaranth in dicamba-tolerant crops, field trials were conducted in 2017 and 2018 at the Lon Mann Cotton Research Station near Marianna, AR, and on-farm in Marion, AR. The experiment included split plot factors of dicamba rate, nozzle type, and carrier volume, with a whole plot factor of population. Dicamba was applied at 560 or 1120 g ae ha−1 through 110015 TTI or AirMix nozzles at 70 or 140 L ha−1 to PPO-resistant or PPO-susceptible Palmer amaranth. Palmer amaranth control 14 d after treatment (DAT) was influenced by an interaction between population and carrier volume. PPO-resistant Palmer amaranth control 14 DAT was 81% regardless of carrier volume, compared with 90% and 95% control at 70 and 140 L ha−1, respectively, of the PPO-susceptible population. An interaction between nozzle type and carrier volume influenced Palmer amaranth control 21 DAT, whereas AirMix nozzles at 140 L ha−1 controlled Palmer amaranth at a greater level (94%) than any other nozzle and carrier volume combination (≤90%). An interaction between population and dicamba rate influenced the relative density of Palmer amaranth 21 DAT. PPO-resistant Palmer amaranth density was less affected by dicamba at either rate than PPO-susceptible Palmer amaranth, relative to the nontreated check. Results concur with those of other research that suggest PPO-resistant Palmer amaranth is harder to control with dicamba. Otherwise, increasing carrier volume affected overall Palmer amaranth control to a greater degree than any other factor.
Highlights
Protoporphyrinogen oxidase (PPO)-inhibiting herbicide-resistant Palmer amaranth was first confirmed in 2011 and is widespread throughout the crop-producing region of Arkansas (Salas et al 2016; Varanasi et al 2018b)
While no mechanisms of resistance to dicamba have been identified in Arkansas Palmer amaranth, the discovery of metabolic resistance mechanisms to other herbicides in Arkansas suggests that metabolic resistance to more herbicide sites of action could be building (Yu and Powles 2014)
The effect of year was not significant for this experiment (P = 0.4653); data across years were analyzed together. Both Palmer amaranth control at 14 and 21 d after treatment (DAT) and Palmer amaranth density 21 DAT were influenced by several two-way interactions and main effects (Table 2)
Summary
Protoporphyrinogen oxidase (PPO)-inhibiting herbicide-resistant Palmer amaranth was first confirmed in 2011 and is widespread throughout the crop-producing region of Arkansas (Salas et al 2016; Varanasi et al 2018b). The resistant populations in this area mostly possess a target-site resistance to all PPO-inhibiting herbicides, as well as resistance to other common herbicides suchas glyphosate and acetolactate synthase (ALS)-inhibiting chemistries (Heap 2019; Varanasi et al 2018b). Metabolic resistance to the very-long-chain fatty acid inhibitor S-metolachlor was identified in Arkansas (Brabham et al 2019). While no mechanisms of resistance to dicamba have been identified in Arkansas Palmer amaranth, the discovery of metabolic resistance mechanisms to other herbicides in Arkansas suggests that metabolic resistance to more herbicide sites of action could be building (Yu and Powles 2014)
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