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Molecular Basis of Resistance to Tribenuron in Water Starwort (Myosoton aquaticum) Populations from China

Published online by Cambridge University Press:  20 January 2017

Weitang Liu
Key Laboratory of Pesticide Toxicology and Application Technique, College of Plant Protection, Shandong Agricultural University, Shandong Tai'an 271018, PR China
Yaling Bi
College of Plant Science, Anhui Science and Technology University, Anhui Fengyang, 233100, PR China
Lingxu Li
College of Chemistry and Pharmacy Science, Qingdao Agricultural University, Shandong Qingdao 266109, PR China
Guohui Yuan
Key Laboratory of Pesticide Toxicology and Application Technique, College of Plant Protection, Shandong Agricultural University, Shandong Tai'an 271018, PR China
Jinxin Wang*
Key Laboratory of Pesticide Toxicology and Application Technique, College of Plant Protection, Shandong Agricultural University, Shandong Tai'an 271018, PR China
Corresponding author's E-mail:


Populations of water starwort, a winter annual or biennial weed in the pink family (Caryophyllaceae), can no longer be controlled by tribenuron following successive use of this herbicide over several years. Whole-plant bioassays have established that the resistant water starwort populations JS17, JS08, JS16, and JS07 showed high-level (from 203-fold to 565-fold) resistance to tribenuron. In vitro acetolactate synthase (ALS) assays revealed that resistance was due to reduced sensitivity of the ALS enzyme to tribenuron. The half-maximal inhibitory concentration (I50) values for JS17, JS08, JS16, and JS07 were 72, 71, 70, and 76 times greater, respectively, than were those of the susceptible population JS24. This altered ALS sensitivity in the resistant populations was due to a mutation in the ALS gene resulting in a Pro197 to Ser substitution (JS17, JS08, and JS16) and a Pro197 to Leu substitution (JS07). This study established the first documented case, to our knowledge, of evolved tribenuron resistance in water starwort and concluded that the molecular basis of resistance is due, at least in part, to a target-site modification at Pro197 in the ALS gene.

Physiology, Chemistry, and Biochemistry
Copyright © Weed Science Society of America 

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