Target-Site and Metabolic Resistance Mechanisms to Penoxsulam in Barnyardgrass (Echinochloa crus-galli (L.) P. Beauv)

Abstract

Herbicide resistance identification is essential for effective chemical weed control. In this study, we quantified the differences in growth response between penoxsulam resistant (R) and sensitive (S) Echinochloa crus-galli populations, explored the changes in ALS, and performed genetic analyses to identify metabolic genes that are up-regulated by the application of penoxsulam and other common herbicides. The R population showed a 26.0-fold higher resistance to penoxsulam and varied resistance to most tested herbicides with indices ranging from 4.9 to 145.9. A Trp-574-Arg amino acid mutation in ALS and low penoxsulam ALS sensitivity were the main mechanisms underlying herbicide resistance. The penoxsulam resistance can be significantly reversed by two P450s inhibitors and one GST inhibitor. By RNA-Seq, thirty-six highly expressed contigs were selected, and 30 of them were up-regulated in the R population treated by penoxsulam. Many of these genes were significantly expressed when treated with pyroxsulam, metamifop, and quinclorac. These upregulated genes appear to be complementary for plant resistance to penoxsulam and other common herbicides.

Differences in efficacy, resistance mechanism and target protein interaction between two PPO inhibitors in Palmer amaranth (Amaranthus palmeri)

“…Finally, NTSR for PPO inhibitors has been reported and can potentially be reversed by application of metabolism inhibitors (Obenland et al 2019;Varanasi et al 2019). Furthermore, NTSR and TSR mechanisms can act together simultaneously, endowing weeds with higher levels of resistance to PPO inhibitors, as has been reported in weeds that are resistant to other herbicide groups (Alcántara-de la Cruz et al 2017;Fang et al 2019).Therefore, future research should aim at uncoupling NTSR mechanisms for PPO inhibitors from TSR mechanisms and at elucidating the concerted roles of these two types of resistance mechanisms in a single weed population. Figure 7.…”

Recurrent Selection by Herbicide Sublethal Dose and Drought Stress Results in Rapid Reduction of Herbicide Sensitivity in Junglerice

“…The cytochrome P450 monooxygenase superfamily is frequently associated with metabolic resistance to herbicides; it is responsible for the phase I metabolism of xenobiotics, including herbicides [21,28,[71][72][73][74][75][76]. The upregulation of CytP450 genes identified here suggests their involvement in the evolution of resistance to florpyrauxifen-benzyl, glyphosate, or quinclorac and adaptation to drought stress.…”

Non-Target-Site Resistance to Herbicides: Recent Developments

“…Interestingly, several cases of coexistence of these mechanisms have been reported. For instance, ALS-inhibitor-resistant water chickweed [33] and barnyard grass [147], ACCase-inhibitor-resistant Vulpia bromoides [148], Italian ryegrass [19], short awn foxtail [41], PS-II inhibitor-resistant wild radish [62], EPSPS-inhibitor-resistant rigid ryegrass [74], common waterhemp [73], HPPD-inhibitor-resistant Palmer amaranth [99], and microtubule inhibitor-resistant rigid ryegrass [34] have been identified with TSR and NTSR mechanisms in the same populations. Therefore, if TSR mechanisms are found to contribute to herbicide resistance, it is also necessary to investigate the NTSR mechanisms and vice versa.…”