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Evolution of target and non-target based multiple herbicide resistance in a single Palmer amaranth (Amaranthus palmeri) population from Kansas

Published online by Cambridge University Press:  29 June 2020

Sushila Chaudhari
Affiliation:
Assistant Professor, Department of Horticulture, Michigan State University, East Lansing, MI, USA
Vijay K. Varanasi
Affiliation:
Senior Biologist, Bayer Crop Science, Chesterfield, MO, USA
Sridevi Nakka
Affiliation:
Scientist, Heartland Plant Innovations, Manhattan, KS, USA
Prasanta C. Bhowmik
Affiliation:
Professor, Weed Science, Stockbridge School of Agriculture, University of Massachusetts, Amherst, MA, USA
Curtis R. Thompson
Affiliation:
Extension Specialist and Professor Emeritus, Department of Agronomy, Kansas State University, Manhattan, KS, USA
Dallas E. Peterson
Affiliation:
Professor, Department of Agronomy, Kansas State University, Manhattan, KS, USA
Randall S. Currie
Affiliation:
Associate Professor, Kansas State University, Southwest Research–Extension Center, Garden City, KS, USA
Mithila Jugulam*
Affiliation:
Associate Professor and Weed Scientist, Department of Agronomy, Kansas State University, Manhattan, KS, USA
*
Author for correspondence: Mithila Jugulam, Department of Agronomy, 2004 Throckmorton PSC, 1712 Claflin Road, Kansas State University, Manhattan, KS66506-0110. Email: mithila@ksu.edu

Abstract

The evolution of resistance to multiple herbicides in Palmer amaranth is a major challenge for its management. In this study, a Palmer amaranth population from Hutchinson, Kansas (HMR), was characterized for resistance to inhibitors of photosystem II (PSII) (e.g., atrazine), acetolactate synthase (ALS) (e.g., chlorsulfuron), and EPSP synthase (EPSPS) (e.g., glyphosate), and this resistance was investigated. About 100 HMR plants were treated with field-recommended doses (1×) of atrazine, chlorsulfuron, and glyphosate, separately along with Hutchinson multiple-herbicide (atrazine, chlorsulfuron, and glyphosate)–susceptible (HMS) Palmer amaranth as control. The mechanism of resistance to these herbicides was investigated by sequencing or amplifying the psbA, ALS, and EPSPS genes, the molecular targets of atrazine, chlorsulfuron, and glyphosate, respectively. Fifty-two percent of plants survived a 1× (2,240 g ai ha−1) atrazine application with no known psbA gene mutation, indicating the predominance of a non–target site resistance mechanism to this herbicide. Forty-two percent of plants survived a 1× (18 g ai ha−1) dose of chlorsulfuron with proline197serine, proline197threonine, proline197alanine, and proline197asparagine, or tryptophan574leucine mutations in the ALS gene. About 40% of the plants survived a 1× (840 g ae ha−1) dose of glyphosate with no known mutations in the EPSPS gene. Quantitative PCR results revealed increased EPSPS copy number (50 to 140) as the mechanism of glyphosate resistance in the survivors. The most important finding of this study was the evolution of resistance to at least two sites of action (SOAs) (~50% of plants) and to all three herbicides due to target site as well as non–target site mechanisms. The high incidence of individual plants with resistance to multiple SOAs poses a challenge for effective management of this weed.

Type
Symposium
Copyright
© Weed Science Society of America, 2020

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