About this Research Topic
It is now clear that herbicide-resistant (HR) weeds constitute a major threat to sustainable food production. A concerning type of resistance mechanism in HR weeds is non-target site resistance (NTSR). NTSR describes mechanisms of resistance that are not directly associated with changes to the herbicide-specific enzyme target site. NTSR can confer increased activity of enzymes involved in herbicide metabolism, which is particularly concerning because it may confer cross-resistance to herbicides with different chemical properties. Consequently, herbicides that have never been applied before might activate resistance in HR-weed genotypes. For these reasons, it is crucial to fully understand the molecular, biochemical, cellular, and physiological mechanisms that lead to NTSR. This knowledge will allow the design of new strategies and detection tools to control HR weeds, aiding the integrated management of HR weeds.
NTSR affects different enzyme families of plant catabolic routes in plant primary metabolism; the main targets are the cytochrome P450 enzymatic complex (phase I) and the glutathione-S-transferase and glycosyltransferase enzyme families (phase II). The potential responses coordinated by these enzymes are yet to be unravelled. New research suggests that the selection pressure exerted by one herbicide on one specific gene could simultaneously select the differential expression of other resistance-conferring genes. Although the proteins responsible for inactivating or sequestering different herbicides may differ, the mechanism of herbicide metabolism that confers cross-resistance might be common. Recent research has discovered another class of enzymes, aldo-keto reductases, which are involved in the metabolism of glyphosate and confer glyphosate resistance. This evidence should stimulate a search for other glyphosate-metabolizing enzymes.
Other enzymes, such as peroxidases, are involved in different mechanisms leading to herbicide resistance. Peroxidases protect plants from herbicide damage and seem to be responsible for NTSR and conferring cross-resistance. Similarly, ABC transporters (phase III) are linked to reduced transport/sequestration of some herbicides. These transporters have several known substrates, and this raises the possibility that they may be involved in translocating different herbicides. An additional question that naturally arises is what resistant plants do with herbicides: are they inactivated in planta, sequestered or secreted? NTSR mechanisms can act alongside TSR mechanisms building up the resistance response. Combined NTSR and TSR mechanisms, such as increased metabolic activity coupled with root exudation, could enable plants to promote herbicide elimination. Other hypothesized modes of action contributing to herbicide resistance mechanisms include epigenetic control and circadian control.
The above-mentioned questions point to several potential mechanisms of herbicide resistance that need to be addressed in future research towards safeguarding food production together with judicious use of herbicides. This Research Topic aims to collect:
• Latest research identifying and characterizing the enzymes and genes involved in enhanced metabolism (increased herbicide metabolism)
• Studies unravelling new NTSR mechanisms that could also confer cross and multiple herbicide resistance
• Studies reporting new cases of multiple herbicide resistance weeds worldwide together with the mechanistic insights behind them.
Keywords: Non-target site resistance, Herbicide-resistant weeds, Metabolism, Multiple resistant weeds, Cross resistance
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