Skip to main content
ARS Home » Southeast Area » Stoneville, Mississippi » Crop Production Systems Research » Research » Publications at this Location » Publication #325760

Research Project: Biology and Management of Herbicide-Resistant Weeds

Location: Crop Production Systems Research

Title: Characterization of Fenoxaprop-P resistant Echinochloa colona from Mississippi

Author
item Wright, Alice
item Nandula, Vijay
item GRIER, LOGAN - Basf Corporation North America
item SHOWMAKER, KURT - Mississippi State University
item BOND, JASON - Mississippi State University
item PETERSON, DANIEL - Mississippi State University
item Ray, Jeffery - Jeff
item SHAW, DAVID - Mississippi State University

Submitted to: Weed Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/15/2016
Publication Date: 1/20/2017
Citation: Wright, A.A., Nandula, V.K., Grier, L., Showmaker, K.C., Bond, J.A., Peterson, D.G., Ray, J.D., Shaw, D.R. 2017. Characterization of Fenoxaprop-P resistant Echinochloa colona from Mississippi. Weed Science. 61,4:588-595. https://doi.org/10.1614/WS-D-16-00024.1.
DOI: https://doi.org/10.1614/WS-D-16-00024.1

Interpretive Summary: Echinochloa colona (jungle rice) is one of the most problematic weeds in rice producing acres of the US Midsouth. A population of junglerice from Sunflower County, MS, exhibited multiple resistance to various herbicides including fenoxaprop-P. Scientists from Mississippi State University, Crop Production Systems Research Unit (USDA-ARS), BASF, and Crop Genetics Research Unit (USDA-ARS) conducted laboratory and greenhouse studies to understand magnitude and why junglerice is resistant to fenoxaprop. An 11 fold difference in ED50 (the effective dose needed to reduce growth by 50%) values was observed when comparing the resistant population (249 g ae ha-1) with susceptible plants (20 g ha-1) collected from a different field. The resistant population was controlled by clethodim and sethoxydim, indicating that while this population is resistant to at least one aryloxyphenoxyproprionate, it is not resistant to cyclohexanedione herbicides. Sequencing of the acetyl coenzyme A carboxylase, which encodes the enzyme targeted by fenoxaprop-P, did not reveal the presence of any known resistance-conferring point mutations. An enzyme assay confirmed that the acetyl coenzyme A carboxylase in the resistant population is herbicide sensitive. Further investigations with two cytochrome P450 inhibitors, malathion and piperonyl butoxide, and a glutathione-S-transferase inhibitor, 4-chloro-7-nitrobenzofurazan, did not indicate involvement of any metabolic enzymes inhibited by these compounds. The absence of a known target-site point mutation and the sensitivity of the ACCase enzyme to herbicide show that fenoxaprop-P resistance in this population is due to a non-target site mechanism. The above findings will provide valuable knowledge towards devising alternative junglerice control strategies for rice growers of the Midsouth.

Technical Abstract: A population of junglerice from Sunflower County, MS, exhibited resistance to fenoxaprop-P. An 11 fold difference in ED50 (the effective dose needed to reduce growth by 50%) values was observed when comparing the resistant population (249 g ae ha-1) with susceptible plants (20 g ha-1) collected from a different field. The resistant population was controlled by clethodim and sethoxydim, indicating that while this population is resistant to at least one aryloxyphenoxyproprionate, it is not resistant to cyclohexanedione herbicides. Sequencing of the acetyl coenzyme A carboxylase, which encodes the enzyme targeted by fenoxaprop-P, did not reveal the presence of any known resistance-conferring point mutations. An enzyme assay confirmed that the acetyl coenzyme A carboxylase in the resistant population is herbicide sensitive. Further investigations with two cytochrome P450 inhibitors, malathion and piperonyl butoxide, and a glutathione-S-transferase inhibitor, 4-chloro-7-nitrobenzofurazan, did not indicate involvement of any metabolic enzymes inhibited by these compounds. The absence of a known target-site point mutation and the sensitivity of the ACCase enzyme to herbicide show that fenoxaprop-P resistance in this population is due to a non-target site mechanism.