Acetyl‐CoA Carboxylase Herbicide Tolerance in Bermudagrass. (1st May 2014)

• Record Type: Journal Article
• Authors: Grimshaw, Austin L.; Schwartz, Brian M.; Grey, Timothy L.; McCullough, Patrick E.; Raymer, Paul L.; Webster, Theodore M.; Kowalewski, A.R.; Tate, Trent M.; Parrott, Wayne A.
• Is Part Of: Agronomy Journal. Volume 106:Number 3(2014)
• Page Start: 925
• Page End: 930
• Publication Date: 2014-05-01
• Subjects: Agronomy -- Periodicals; 630
• DOI: 10.2134/agronj13.0423
• Languages: English
• ISSNs: 0002-1962

Abstract

Abstract : Contamination of newly planted bermudagrass ( Cynodon spp.) varieties by undesirable off‐type bermudagrass genotypes is an ever increasing concern for turf managers because selective control options are limited. In 2009, a sethoxydim {2‐[1‐(ethoxyimino)butyl]‐5‐[2‐(ethylthio)propyl]‐3‐hydroxy‐2‐cyclohexen‐1‐one} tolerant bermudagrass genotype (93‐175) was identified during herbicide screening at the University of Georgia in Tifton. The objective of this research was to assess the tolerance of 93‐175 to three Acetyl‐CoA carboxylase (ACCase) herbicides in comparison to the susceptible genotypes Tifway and common bermudagrass. Greenhouse and field trials were performed between August 2011 and April 2013. Factors in the field experiment included ACCase herbicides, application rates, bermudagrass genotypes, and locations. Turfgrass injury ratings taken 42 days after treatment (DAT) and during greenup the following spring supported initial preliminary findings. At the 1x rate of sethoxydim (280 g a.i. ha −1 ), 93‐175 displayed 50 to 87% less injury in comparison to the susceptible genotypes. In the spring of 2013, 93‐175 plots treated with a 1x rate of sethoxydim reached 100% recovery during the same time period as non‐treated controls, while common and Tifway had only recovered to 48 and 60%, respectively. The tolerance mechanism of 93‐175 to sethoxydim did not confer an appreciable reduction of clethodim {( E, E )‐(6)‐2‐[1‐[[(3‐chloro‐2‐propenyl)oxy]imino]propyl]‐5‐[2‐(ethylthio)propyl]‐3‐hydroxy‐2‐cyclohexen‐1‐one} or fluazifop {(6)‐2‐[4‐[[5‐(trifluoromethyl)‐2‐pyridinyl]oxy]phenoxy]propanoic acid} herbicide treatment effects. 93‐175 will continue to be studied to determine transferability of herbicide tolerance to progeny and the mechanism of the observed tolerance.