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−1 for creeping bentgrass, Kentucky
bluegrass, and goosegrass, respectively. The GR50 for
bermudagrass treated with diclofop-methyl or metamifop was 2,850 and 60 g
ha−1, respectively. In laboratory experiments, peak absorption
of 14C-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% of
14C-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 of 14C-metamifop in bermudagrass
was similar to 14C-diclofop-methyl. Bermudagrass metabolized 23
and 60% of the absorbed 14C-diclofop-methyl to diclofop acid and
a polar conjugate after 96 h, respectively, but only 14% of
14C-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.