Abstract

Papaver rhoeas biotypes displaying multiple herbicide resistance to ALS inhibitors and synthetic auxin herbicides (SAH) are spreading across Europe. In Spain, enhanced metabolism to imazamox was confirmed in one population, while cytochrome-P450 (P450) based metabolism to 2,4-D in another two. The objectives of this research were to further confirm the presence of P450 mediated enhanced metabolism and, if so, to confirm whether a putative common P450 is responsible of metabolizing both 2,4-D and imazamox. Metabolism studies were undertaken in five P. rhoeas populations with contrasted HR profiles (herbicide susceptible, only HR to ALS inhibitors, only HR to SAH, or multiple HR to both), and moreover, three different P450 inhibitors were used. The presence of enhanced metabolism to these SoA was confirmed in three more HR P. rhoeas populations. This study provides the first direct evidence that imazamox metabolism in these biotypes is P450-mediated, also in one population without an altered target site. Additionally, it was further confirmed that enhanced metabolism of 2,4-D in biotypes only HR to SAH or multiple HR to ALS inhibitors and SAH involves P450 as well. No metabolism was detected using the three inhibitors in all the herbicide-metabolizing P. rhoeas biotypes, suggesting that a common metabolic system involving P450s is responsible of degrading herbicides affecting both SoAs. Thus, selection pressure with either SAH or imidazolinone ALS inhibitors can select not only for resistance to each of them, but it can also confer cross-resistance between them in P. rhoeas.

Highlights

  • Non-target site resistance (NTSR) is any mechanism not related with the herbicide target in contrast with target site resistance (TSR)

  • The polygenic nature of cytochrome P450 mono-oxygenases (P450s) metabolism-based herbicide resistance has already been demonstrated (Busi et al, 2011). Enhanced metabolism both to acetolactate synthase (ALS) inhibiting herbicides and synthetic auxin herbicides (SAH) (2,4-D) was confirmed in herbicide resistant (HR) P. rhoeas populations, and strong proofs were provided that is primarily P450-based in both sites of action (SoA)

  • This study provided the first direct evidences that imazamox metabolism is mediated by P450 and confirmed previous studies that enhanced metabolism to SAH involved this enzyme family too

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Summary

Introduction

Non-target site resistance (NTSR) is any mechanism not related with the herbicide target in contrast with target site resistance (TSR). The most con­ cerning type of NTSR in herbicide resistant (HR) weeds are enhanced rates of herbicide metabolism, because they may confer cross-resistance to herbicides with different SoA (Rigon et al, 2020). Constitutive enzymatic super families are respon­ sible for these different four phases: e.g., cytochrome P450 mono-oxygenases (P450s) in phase I, glutathione-S-transferases (GSTs) and glucosyltransferases (GTs) in phase II, and ABC transporters in phase III, and others (Gaines et al, 2020). P450s are probably the most researched detoxifying enzymes in HR weeds up-to-date and they play a primary role in the Phase I metabolism of herbicides. P450s can confer NTSR to weeds by means of enhanced degradation rates to several SoA (Siminszky, 2006)

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