Resistance to Acetolactate Synthase Inhibitors in a Biotype of Monochoria vaginalis Discovered in Korea

Author： Hwang I.T.   Lee K.H.   Park S.H.   Lee B.H.   Hong K.S.   Han S.S.   Cho K.Y.  

Publisher： Academic Press

ISSN： 0048-3575

Source： Pesticide Biochemistry and Physiology, Vol.71, Iss.2, 2001-10, pp. : 69-76

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Abstract

A Monochoria vaginalis population that survived after treatment with sulfonylurea herbicide-based mixtures was identified in 1997 in the paddy fields in Chonnam province, Korea. The field had been in monoculture rice production and had been treated with sulfonylurea herbicide-based mixtures for 8 consecutive years. In greenhouse studies, the resistant/wild I50 ratios of M. vaginalis to pyrazosulfuron-ethyl were 21.2, 28.5, 23.4, and 12.8 when treated at 2, 7, 14, and 21 days after seeding, respectively. The same trends of I50 ratios of 42.4, 17.2, 9.2, and 6.1 were obtained after treatment with bensulfuron-methyl, respectively. The resistant type of M. vaginalis showed high levels of cross-resistance to pyrazosulfuron-ethyl, bensulfuron-methyl, 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, butachlor, and 2,4-D. In vitro acetolactate synthase (ALS) assay showed that the pI50 values of bensulfuron-methyl to the wild and resistant type of M. vaginalis were 9.3 and 7.1. Also, the pI50 values of flumetsulam to the wild and resistant type of M. vaginalis were 7.7 and 6.0 but those of imazaquin were 8.3 and 8.2. Acetolactate accumulation in the resistant type of M. vaginalis plants treated with bensulfuron-methyl 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 treated with imazaquin was not significantly different in the wild and the resistant type of M. vaginalis. In vitro and in vivo ALS assay results showed that the resistance mechanism of M. vaginalis might be due to the altered acetolactate synthase.

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