|RIAR, DILPREET - University Of Arkansas|
|NORSWORTHY, JASON - University Of Arkansas|
|SRIVASTAVA, VIBHA - University Of Arkansas|
|BOND, JASON - Delta Research & Extension Center|
|SCOTT, ROBERT - University Of Arkansas|
Submitted to: Journal of Agricultural and Food Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/13/2012
Publication Date: 12/13/2012
Citation: Riar, D.S., Norsworthy, J.K., Srivastava, V., Nandula, V.K., Bond, J.A., Scott, R.C. 2012. Physiological and molecular basis of acetolactate synthase-inhibiting herbicide resistance in barnyardgrass (Echinochloa crus-galli). Journal of Agricultural and Food Chemistry. 61:278-289.
Interpretive Summary: Several populations of barnyardgrass, an important weed in rice production systems of the Midsouth (Arkansas, Louisiana, Mississippi), have developed resistance to various acetolactate synthase (ALS)-inhibiting herbicides, thereby, making management matters worse. Scientists from the University of Arkansas, Crop Production Systems Research Unit (USDA-ARS), and Mississippi State University conducted laboratory and greenhouse studies to understand why barnyardgrass populations are resistant to one or more ALS-inhibiting herbicides. Molecular analysis of the ALS coding sequence showed an Ala122 to Val and Ala122 to Thr substitution in two resistant biotypes from Arkansas resulting in resistance to imazamox. Translocation or movement of bispyribac and/or imazamox was less in two resistant biotypes, one each from Arkansas and Mississippi compared to a susceptible biotype. These results indicate that the mechanism of resistance to imazamox in at least one of the resistant biotypes from Arkansas is due to mutation on the ALS enzyme. Also, resistance to imazamox and bispyribac is due to reduced movement of the herbicide to sensitive tissues in one of the resistant biotypes from Arkansas and a resistant biotype from Mississippi. The above findings will provide valuable knowledge towards devising alternative barnyardgrass control strategies and minimizing impact on rice growers of the Midsouth.
Technical Abstract: Barnyardgrass biotypes from Arkansas (AR1 and AR2) and Mississippi (MS1) have evolved cross-resistance to imazamox, imazethapyr, and penoxsulam. Additionally, AR1 and MS1 have evolved cross-resistance to bispyribac-sodium. Studies were conducted to determine if reduced translocation or altered target site is a mechanism of resistance to acetolactate synthase (ALS)-inhibiting herbicides in these resistant biotypes. Sequencing and analysis of a 1701 base pair ALS coding sequence revealed an Ala122 to Val and Ala122 to Thr substitution in AR1 and AR2, respectively. The imazamox concentrations required for 50% inhibition of ALS enzyme activity in vitro of AR1 and AR2 were 2.0 and 5.8 times, respectively, greater than the susceptible biotype. Absorption of 14C-bispyribac-sodium, -imazamox, and -penoxsulam was similar in all biotypes. 14C-penoxsulam translocation out of the treated leaf (<2%) was similar among all biotypes. 14C-bispyribac-treated AR1 and MS1 translocated 31 to 43% less radioactivity to aboveground tissue below the treated leaf compared to the susceptible biotype. 14C-imazamox-treated AR1 plants translocated 39% less radioactivity above the treated leaf and aboveground tissue below the treated leaf, and MS1 translocated 54 and 18% less radioactivity to aboveground tissue above and below the treated leaf, respectively, compared to the susceptible biotype. This study shows that altered target site is a mechanism of resistance to imazamox in AR2 and probably in AR1. Additionally, reduced translocation partially contributes to imazamox and bispyribac-sodium resistance in AR1 and MS1.