Resistance to acetolactate synthase inhibitors in a biotype of Monochoria vaginalis discovered in Korea

A Monochoria vaginalis population that survived after treatment with sulfon ylurea herbicide-based mixtures was identified in 1997 in the paddy fields in Chonnam province, Korea. The field had been in monoculture rice producti on and had been treated with sulfonylurea herbicide-based mixtures for 8 co nsecutive years. In greenhouse studies, the resistant/wild I-50 ratios of M . vaginalis to pyrazosulfuron-ethyl were 21.2, 28.5, 23.4, and 12.8 when tr eated at 2, 7, 14, and 21 days after seeding, respectively. The same trends of 150 ratios of 42.4, 17.2, 9.2, and 6.1 were obtained after treatment wi th bensulfuron-methyl, respectively. The resistant type of M. vaginalis sho wed high levels of cross-resistance to pyrazosulftiron-ethyl, bensulfuronme thyl, cyclosulfamuron, and flumetsulam, but not to imazaquin. The resistant type of M. vaginalis did not show multiple resistance to other herbicides having different modes of action, such as simazine, propanil, oxadiazon, bu tachlor, and 2,4-D. In vitro acetolactate synthase (ALS) assay showed that the pI(50) values of bensulfuron-methyl to the wild and resistant type of M . vaginalis were 9.3 and 7. 1. Also, the pI(50) values of flumetsulam to th e wild and resistant type of M. vaginalis were 7.7 and 6.0 but those of ima zaquin were 8.3 and 8.2. Acetolactate accumulation in the resistant type of M. vaginalis plants treated with bensulfuronmethyl or flumetsulam followed by 1,1-cyclopropane dicarboxylic acid were significantly higher than that of wild type. However, the accumulation of acetolactate in the plants treat ed with imazaquin was riot significantly different in the wild and the resi stant type of M. vaginalis. In vitro and in vivo ALS assay results showed t hat the resistance mechanism of M. vaginalis might be due to the altered ac etolactate synthase.