Abstract
Bermudagrass and goosegrass are problematic weeds with limited herbicides available for POST control in creeping bentgrass. Metamifop effectively controls these weeds with greater selectivity in cool-season grasses than other ACCase inhibitors. The objectives of this research were to determine the physiological basis for metamifop selectivity in turfgrasses. In greenhouse experiments, metamifop rate required to reduce shoot biomass 50% from the nontreated (GR50) at 4 wk after treatment was > 6,400, 2,166, and 53 g ai ha−1for creeping bentgrass, Kentucky bluegrass, and goosegrass, respectively. The GR50for bermudagrass treated with diclofop-methyl or metamifop was 2,850 and 60 g ha−1, respectively. In laboratory experiments, peak absorption of14C-metamifop was reached at 48, 72, and 96 h after treatment (HAT) for goosegrass, creeping bentgrass and Kentucky bluegrass, respectively. Grasses translocated < 10% of the absorbed radioactivity out of the treated leaf at 96 HAT, but creeping bentgrass translocated three times more radioactivity than goosegrass and Kentucky bluegrass. Creeping bentgrass, Kentucky bluegrass, and goosegrass metabolized 16, 14, and 25% of14C-metamifop after 96 h, respectively. Goosegrass had around two times greater levels of a metabolite at retention factor 0.45 than creeping bentgrass and Kentucky bluegrass. The concentration of metamifop required to inhibit isolated ACCase enzymes 50% from the nontreated (I50) measured > 100, > 100, and 38 μM for creeping bentgrass, Kentucky bluegrass, and goosegrass, respectively. In other experiments, foliar absorption of14C-metamifop in bermudagrass was similar to14C-diclofop-methyl. Bermudagrass metabolized 23 and 60% of the absorbed14C-diclofop-methyl to diclofop acid and a polar conjugate after 96 h, respectively, but only 14% of14C-metamifop was metabolized. Isolated ACCase was equally susceptible to inhibition by diclofop acid and metamifop (I50= 0.7 μM), suggesting degradation rate is associated with bermudagrass tolerance levels to these herbicides. Overall, the physiological basis for metamifop selectivity in turfgrass is differential levels of target site inhibition.
Highlights
14C-fixation was determined by substituting degassed, deionized water for acetyl-CoA
The objective of this research was to evaluate the physiological basis for metamifop selectivity for bermudagrass and goosegrass control in cool-season turfgrasses
‘Princess’ bermudagrass (Pennington Seed Inc., Madison, GA 30650), ‘Penn A-4’ creeping bentgrass (Tee-2-Green Corp., Hubbard, OR 97032), ‘Midnight’ Kentucky bluegrass (Preferred Seed, Buffalo, NY 14227), and goose‐ grass were seeded in pots at the University of Georgia (UGA) Griffin Campus
Summary
14C-fixation (nonenzymatic 14CO2 fixation) was determined by substituting degassed, deionized water for acetyl-CoA. The radioactivity fixed to malonyl-CoA was quantified by liquid scintillation spectroscopy. The concentration of herbicide required to cause 50% inhibition of ACCase activity (I50) was determined from concentration response curves. The susceptibility of isolated ACCase enzymes of bermudagrass to inhibition by diclofop acid and metamifop was evaluated using the aforementioned methodology. Concentrations of the medium solutions evaluated contained 0.1, 1, 10, or 100 mM of either herbicide. Radioactivity fixed to malonyl-CoA was quantified as previously described, and I50 values were determined from the concentration–response curves
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