Point Mutations as Main Resistance Mechanism Together With P450-Based Metabolism Confer Broad Resistance to Different ALS-Inhibiting Herbicides in Glebionis coronaria From Tunisia

Abstract

Resistance to acetolactate synthase (ALS) inhibiting herbicides has recently been reported in Glebionis coronaria from wheat fields in northern Tunisia, where the weed is widespread. However, potential resistance mechanisms conferring resistance in these populations are unknown. The aim of this research was to study target-site resistance (TSR) and non-target-site resistance (NTSR) mechanisms present in two putative resistant (R) populations. Dose–response experiments, ALS enzyme activity assays, ALS gene sequencing, absorption and translocation experiments with radiolabeled herbicides, and metabolism experiments were carried out for this purpose. Whole plant trials confirmed high resistance levels to tribenuron and cross-resistance to florasulam and imazamox. ALS enzyme activity further confirmed cross-resistance to these three herbicides and also to bispyribac, but not to flucarbazone. Sequence analysis revealed the presence of amino acid substitutions in positions 197, 376, and 574 of the target enzyme. Among the NTSR mechanisms investigated, absorption or translocation did not contribute to resistance, while evidences of the presence of enhanced metabolism were provided. A pretreatment with the cytochrome P450 monooxygenase (P450) inhibitor malathion partially synergized with imazamox in post-emergence but not with tribenuron in dose–response experiments. Additionally, an imazamox hydroxyl metabolite was detected in both R populations in metabolism experiments, which disappeared with the pretreatment with malathion. This study confirms the evolution of cross-resistance to ALS inhibiting herbicides in G. coronaria from Tunisia through TSR and NTSR mechanisms. The presence of enhanced metabolism involving P450 is threatening the chemical management of this weed in Tunisian wheat fields, since it might confer cross-resistance to other sites of action.

A Target-Site Mutation Confers Cross-Resistance to ALS-Inhibiting Herbicides in Erigeron sumatrensis from Brazil

“…However, in the R population of E. sumatrensis, there was no synergism between the tested ALS-inhibiting herbicides and the organophosphate malathion, which indicates that ALS inhibitors metabolism by P450 enzymes is not the mechanism involved in the resistance of this population. Malathion may not inhibit all P450 enzymes, and then, further investigations are necessary since metabolism can simultaneously contribute with other mechanisms of ALS-resistant plants [24].…”

Herbicide Resistance of Centaurea cyanus L. in Poland in the Context of Its Management

“…The tests revealed cross-resistance patterns to sulfonylurea herbicides, i.e., tribenuron, chlorsulfuron and sulfometuron, and to an imidazolinone herbicide, i.e., imazapyr. Cross-resistance to other ALS inhibitors is commonly found in weed species [33,52,53]. P. rhoeas is another broadleaved weed species causing problems in winter cereals owing to herbicide resistance.…”

Non-Target-Site Resistance Mechanisms Endow Multiple Herbicide Resistance to Five Mechanisms of Action in Conyza bonariensis

“…Participation of Cyt-P450 in the metabolism of tribenuron-methyl was only partial, allowing that R C. bonariensis plants transformed 58% of the herbicide applied into OH-MM and the conjugate-MM. Metabolism-based resistance to ALS inhibiting herbicides have long been reported and are increasing in both monocot and dicot weed species. , However, there are a few cases in which the metabolism of sulfonylureas has been described as the dominant resistance mechanism in dicot weeds. ,, Because the susceptibility to tribenuron-methyl of the R population did not decrease at the level of the S population with the application of malathion, it is possible that a target site mutation, other metabolic enzyme families, or NTSR mechanisms also participate in the resistance to this herbicide; i.e., resistance to tribenuron-methyl involves TSR and NTSR mechanisms.…”