The University of Tennessee held its annual Weed Tour on June 16 at the West Tennessee AgResearch and Education Center in Jackson. The overarching theme of the day — metabolic weed resistance is here and spreading.

“We’re clearly seeing metabolic resistance,” said Larry Steckel, UT Extension weed specialist. “It’s different than what we’ve always seen with target site resistance, which is what Roundup or PPO resistance was. With target site resistance, it seems like overnight, the herbicide, even applied at six to ten times the labeled rate quits working on a particular weed. While what we have seen with metabolic driven herbicide resistance typically involved more than one herbicide with the level of resistance two to four times.”

“We’re seeing it with dicamba and 2,4-D, but we’re also seeing more subtle declines in control with a number of different herbicides, including the Group 15 herbicides like Dual or Warrant,” he adds. “Not that they’re not working, but maybe they were working for 17 days and now they’re only holding 15-16 days.”

Steckel’s take home message for managing metabolic weed resistance: Use the max rate of pre-emergence herbicide for any given soil type. Then, overlay another pre-emergence herbicide. You’ll need two passes of post-emergence herbicides. Be as timely as you can with those post applications.

Visitors to the Weed Tour were able to see dozens of herbicide treatments in the university’s research plots. The tour was led by Steckel, along with Clay Perkins and graduate student Delaney Foster. In addition to plots at the AgResearch Center, Steckel and his crew conduct on-farm research where they are seeing more evidence of metabolic resistance. Even documenting Palmer amaranth escapes from applications of auxin herbicides made at the 4X rate.

“We’ve got to start thinking about some different ways to manage for it,” he added. “One is to be as timely as possible, which is easier said than done. The other is relying more on pres. Based on my conversations with farmers and retailers, I think we’re using more pre’s this year, and I think that’s helped. They’ve worked for the most part pretty well. But now we’re in the crunch time when all the posts are going out, and I’m expecting some calls from folks who are disappointed in their herbicide performance.”

Combating metabolic weed resistance

Cytochrome P450 is a naturally occurring enzyme that detoxifies foreign chemicals. It’s found in plants and animals, but plants have more genes for the P450 enzyme. Over time growers inadvertently select for weeds with higher numbers of these enzymes in their genetic makeup. These enzymes can then detoxify herbicides applied to the weed.

Researchers often test for metabolic resistance by mixing the herbicide in question with malathion. Malathion, along with all the organophosphate insecticides, are known cytochrome P450 inhibitors. That means they’ll bind up the enzyme that is detoxifying the herbicide.

“When you inhibit those P450’s, the thought is the herbicide will now kill the weed,” Foster said.

Steckel and Foster were hopeful malathion could be a solution. In greenhouse research this past winter, they saw promising results, with malathion improving auxin herbicide control as much as 32% in some treatments. But results in field trials were not as good.

“It worked a little better with 2,4-D than dicamba,” Foster said, “but here we didn’t see a big malathion difference. That doesn’t mean this herbicide resistance isn’t metabolism based. There are hundreds of P450 enzymes and lots of P450 inhibitors. Malathion targets one. We’ll continue evaluating other P450 inhibitors and hopefully figure out what the mechanism of resistance is here.”