Metabolism-based Herbicide Resistance in Weeds

Repeated selection by herbicides results in weed populations evolving various mechanisms that allow them to survive exposure to those herbicides. These mechanisms can be grouped into two categories: those that alter the herbicide binding site (target-site mechanisms) and those that reduce the amount of herbicide reaching the target site or allow the plant to survive despite herbicidal inhibition of the target site (collectively termed nontarget-site mechanisms). Historically, target-site resistance was most common in many of our troublesome weeds (particularly broadleaf weeds, such as waterhemp). Now, however, nontarget-site resistance is becoming more prevalent. Of the various nontarget-site mechanisms, enhanced herbicide metabolism is most common. Compared to target-site resistance, metabolic-based resistance is more complicated. In fact, our understanding of it is still in its infancy. In general, however, metabolic-based resistance is thought to evolve via increased expression in plants of one or more enzymes capable of detoxifying herbicide molecules. The challenge that this creates for weed management is that these enzymes might be able to also detoxify herbicides with other, unrelated modes of action. As an example, a weed population with metabolic resistance to an HPPD-inhibiting herbicide might also be resistant to a herbicide that has yet to be commercialized, even if it has a new mode of action. Furthermore, many of our herbicide-resistance mitigation strategies are based on target-site resistance. For example, mixing two effective herbicides with different sites of action is a great strategy to prevent target-site resistance from occurring but, in some cases, could be completely ineffective in preventing metabolic-based resistance. As metabolic herbicide resistance becomes more common, we are entering a new and more challenging era of herbicide-resistant weeds.