Date of Graduation

12-2017

Document Type

Thesis

Degree Name

Master of Science in Cell & Molecular Biology (MS)

Degree Level

Graduate

Department

Cell & Molecular Biology

Advisor/Mentor

Burgos, Nilda R.

Committee Member

Shi, Ainong

Second Committee Member

Savin, Mary C.

Third Committee Member

Norman, Richard J.

Fourth Committee Member

Rauh, Amy

Keywords

ALS inhibitor; EPSPS inhibitors; Gene copy number; HPPD inhibitor; Mutations; Palmer amaranth

Abstract

Palmer amaranth is a principal weed problem across the United States and is resistant to several herbicide modes of action. By 2008, Palmer amaranth in Arkansas was reported to be resistant to both ALS- and EPSPS-inhibitors, but the predominant resistance mechanisms are yet to be explored. Herbicide options with different modes of action are needed to provide effective Palmer amaranth control and HPPD-inhibitors (e.g. mesotrione) are among these. The goal of this research was to elucidate the resistance profile of Palmer amaranth in Arkansas to ALS herbicides and glyphosate (EPSPS-inhibitor) as well as evaluate the differential tolerance of Palmer amaranth to mesotrione. This research aimed to (1) evaluate the response of Palmer amaranth populations to the full dose of glyphosate and mesotrione; (2) determine if tolerance to mesotrione is heritable; (3) determine the mechanism of resistance to glyphosate in selected accessions; and (4) verify the target-site as the mechanism of resistance in ALS-resistant Palmer amaranth. For objective 1, a total of 119 accessions were collected from crop fields in Arkansas between 2008 and 2014. Overall, 55% of the accessions (115) were glyphosate-resistant (GR). Mesotrione controlled 74% of the accessions (119); the remaining accessions had survivors with high injury (61%-90%). For objective 2, low level of tolerance to mesotrione (3- to 5-fold) was observed in four recalcitrant accessions. For objective 3, 20 accessions were selected. GR accessions had ED50 494 g ha-1 to 1355 g ha-1 and for susceptible accessions ED50 ranged from 28 g ha-1 to 207 g ha-1. EPSPS gene amplification was the primary mechanism of resistance. For objective 4, Palmer amaranth accessions were cross-resistant to pyrithiobac and trifloxysulfuron. Out of 20 accessions, 19 showed 21- to 56-fold resistance to trifloxysulfuron than the susceptible. Four and seven increased ALS copies were observed in a single plant from White and Mississippi counties, respectively, indicating the elevated ALS copies as potential mechanism of resistance in these accessions. Although, all accessions but susceptible had Trp574Ser mutation along with Ala122Thr, Pro197Ala and Ser653Asn present in a few plants, confirming mutations at the target-site as the main mechanism of resistance to ALS-inhibitors.

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