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Characterization of Fenoxaprop-P-Ethyl–Resistant Junglerice (Echinochloa colona) from Mississippi

Published online by Cambridge University Press:  20 January 2017

Alice A. Wright ,
Vijay K. Nandula ,
Logan Grier ,
Kurt C. Showmaker ,
Jason A. Bond ,
Daniel G. Peterson ,
Jeffery D. Ray  and
David R. Shaw
Alice A. Wright*
Affiliation:
Department of Plant and Soil Sciences, Mississippi State University, Mississippi State, MS 39762
Vijay K. Nandula
Affiliation:
Crop Production Systems Research Unit, Agricultural Research Service, Stoneville, MS 38776
Logan Grier
Affiliation:
BASF, RTP, NC 27709
Kurt C. Showmaker
Affiliation:
Institute for Genomics, Biocomputing, and Biotechnology, Mississippi State University, Mississippi State, MS 39762
Jason A. Bond
Affiliation:
Department of Plant and Soil Sciences, Mississippi State University, Mississippi State, MS 39762
Daniel G. Peterson
Affiliation:
Department of Plant and Soil Sciences, Mississippi State University, Mississippi State, MS 39762
Jeffery D. Ray
Affiliation:
Crop Genetics Research Unit, Agricultural Research Service, Stoneville, MS 38776
David R. Shaw
Affiliation:
Department of Plant and Soil Sciences, Mississippi State University, Mississippi State, MS 39762
*
Corresponding author's E-mail: aaw240@msstate.edu
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Abstract

A population of junglerice from Sunflower County, MS, exhibited resistance to fenoxaprop-P-ethyl. 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 ae ha–1) collected from a different field. The resistant population was controlled by clethodim and sethoxydim at the field rate. Sequencing of the acetyl coenzyme A carboxylase, which encodes the enzyme targeted by fenoxaprop-P-ethyl, 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-ethyl resistance in this population is due to a non–target-site mechanism or mechanisms.

Keywords

Clethodimfenoxaprop-P-ethylsethoxydimjunglerice, Echinochloa colona Link. ECHCOAcetyl coenzyme A carboxylaseEchinochloa colonafenoxaprop-P-ethylherbicide metabolism
Type
Physiology/Chemistry/Biochemistry
Information
Weed Science , Volume 64 , Issue 4 , December 2016 , pp. 588 - 595
Copyright
Copyright © 2016 by the Weed Science Society of America 

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Footnotes

Associate editor for this paper: Marie A. Jasieniuk, University of California, Davis.

References

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