|Gaines, Todd -|
|Leach, Jan -|
|Preston, Christopher -|
|Westra, Phil -|
Submitted to: Journal of Agricultural and Food Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 24, 2010
Publication Date: February 17, 2011
Citation: Gaines, T., Shaner, D.L., Leach, J., Preston, C., Westra, P. 2011. Mechanism Of Resistance Of Evolved Glyphosate-Resistant Palmer Amaranth (Amaranthus Palmeri L.). Journal of Agricultural and Food Chemistry. DOI:10,102/JF/047/19K. Interpretive Summary: Weed management is critical for crop production and glyphosate plays a major role in controlling weeds in conventional and glyphosate-resistant crops. The continuous use of glyphosate in glyphosate resistant cotton has led to the selection of populations of Palmer amaranth, a serious weed in cotton production in the U.S. that are resistant to glyphosate. The mechanism of glyphosate resistance in this Palmer amaranth biotype is greatly elevated levels of the target site for the herbicide due to gene duplication. This research further supports the hypothesis that glyphosate resistance in Palmer amaranth is due to gene duplication. Although this is the first known occurrence of gene amplification as an herbicide resistance mechanism in a naturally occurring weed population, it is significant since it could threaten the sustainable use of glyphosate resistant crop technology.
Technical Abstract: Evolved glyphosate resistance in weedy species represents a challenge for the continued success and utility of glyphosate-resistant crops. The first case of evolved glyphosate resistance in Palmer amaranth was a population from the U.S. state of Georgia, which was previously reported to have amplification of the 5-enolpyruvyl shikimate-3-phosphate synthase (EPSPS) gene as the resistance mechanism. Here, we provide additional evidence for the role of EPSPS gene amplification in glyphosate resistance in this population. Increased EPSPS genomic copy number was evident in multiple progeny of crosses involving glyphosate-resistant (R) individuals. Progeny of R by susceptible (S) crosses varied widely for the extent of EPSPS gene amplification, from wild-type EPSPS copy number (no increase in EPSPS relative to a control gene) to over 100-fold amplification. Increased EPSPS copy number was associated with glyphosate resistance in an F2 population. These results further confirm the role of EPSPS gene amplification in conferring glyphosate resistance in this population of Palmer amaranth.