Coupling a soil-applied insecticide with a preemergence herbicide application can – in at least one case – reverse a form of resistance, making population susceptible once again.
In this case, Australian researchers applied a granular form of the insecticide phorate to the soil just before spraying trifluralin. The approach took out a high percentage of the annual ryegrass that carried metabolic resistance to that herbicide.
Nobody is recommending that combination on a commercial basis, but the work provides tantalizing possibilities for tricking resistant weeds in the future or even tailoring new forms of herbicide resistance in commercial crops.
The term “metabolic resistance” rarely turns up in farm publications when editors write about weed resistance. Typically, reports focus on “target site resistance” as the markers for herbicide resistance.
But this lesser mentioned mechanism can contribute to the spread of different types of resistance, Benjamin notes.
“Metabolic resistance is the lesser known cousin to target site resistance in the world of herbicide resistance mechanisms,” Benjamin explained. “Target site resistance is comparatively easy to identify and study, being a more direct ‘cause and effect’ type mechanism that usually confers quite high levels of resistance. Metabolic resistance, however, is more complex and more difficult to study due to many internal mechanisms involving secondary enzyme production and activity.”
While metabolic resistance is often moderate, it can span several groups of herbicidal modes of action. So plants with the right metabolic resistance can tolerate herbicides that they never encountered before.
“This has a dramatic and limiting effect on herbicide choice and makes herbicide rotation a much less powerful control tactic,” Benjamin wrote.
Metabolic Herbicide Resistance Helps Weeds Dodge The Bullet
Simply put, “metabolic resistance occurs when the plant uses its metabolic pathways to produce enzymes that ‘protect’ target sites from the applied herbicide molecules.”
By blocking herbicides from target sites, the herbicide never arrives and the weed dodges the bullet. That same enzyme or multiple enzymes might shield several target sites, leading to plants with cross resistance to multiple chemistries.
In Australian, populations of annual ryegrass in the state of Western Australia have shown high rates of multiple resistance. Upwards of 70% of evaluated populations exhibited both metabolic and target-site resistance.
“Research into gaining a better understanding of one group of enzymes, known as P450s, has uncovered an unlikely synergism between an insecticide and current pre-emergent herbicides to control ryegrass,” Benjamin reports.
Roberto Busi – a scientist with the Australian Herbicide Resistance Initiative (AHRI) – has shown that it is possible in this case to reverse metabolic resistance to trifluralin in annual ryegrass using an organo-phosphate insecticide (phorate).”
Busi also is working in conjunction with Todd Gaines – who studies molecular weed science at Colorado State University – to pinpoint the genetic basis of this metabolic resistance. The goal is to find new ways to control metabolic-resistant weed species.
Metabolic Resistance To Herbicides Can Happen Quickly, Too
To illustrate how rapidly metabolic resistance can become an economic factor, Busi points to pyroxasulfone, which came to market in Australia as a preemergent herbicide in 2012. “Yet even before it was brought to market, research had shown its mode of action can be ‘broken’ within just 3 generations using low application rates… (that can) result in 10-fold resistance.”
Considering that, finding any new modes of action may not be enough if metabolic resistance enters the mix. In his work with trifluralin-resistant annual ryegrass, Busi showed that inhibiting P450 enzyme production reverses resistance with that pre-emergent herbicide.
In his tests, Busi applied a granular formulation of phorate to the soil just before spraying trifluralin. The result: “We were able to prevent establishment of plants with known resistance to trifluralin,” he says.
The research provides a proof-of-concept, says Busi, showing that it’s possible “to manipulate and even reverse metabolic resistance with the use of existing pesticides.”
As Benjamin points out in her report: “Current research is investigating ways to design better P450 inhibitor mechanisms using gene technology and to use these mechanisms in future crop breeding programs to confer crop tolerance to certain herbicides.”