Inheritance of Evolved Glyphosate Resistance in a North Carolina Palmer Amaranth (<i>Amaranthus palmeri</i>) Biotype

Chandi, Aman; Milla‐Lewis, Susana R.; Giacomini, Darci A.; Westra, Philip; Preston, Christopher; Jordan, David L.; York, Alan C.; Burton, J. D.; Whitaker, Jared R.

doi:10.1155/2012/176108

Cited by 52 publications

(75 citation statements)

References 29 publications

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“…In the Georgia A. palmeri population, the EPSPS gene was present on all chromosomes. Subsequently, a North Carolina GR A. palmeri population was reported with EPSPS gene duplication from 22‐ to 63‐fold . A New Mexico GR A. palmeri population was sevenfold more resistant than a GS population and had EPSPS gene duplication ranging from two‐ to tenfold, and individuals with EPSPS gene duplication were able to survive label‐rate glyphosate applications (0.82 kg ha −1 ) …”

Section: Gene Duplicationmentioning

confidence: 99%

Glyphosate resistance: state of knowledge

Sammons

Gaines

2014

Pest Management Science

400

609

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Studies of mechanisms of resistance to glyphosate have increased current understanding of herbicide resistance mechanisms. Thus far, single-codon non-synonymous mutations of EPSPS (5-enolypyruvylshikimate-3-phosphate synthase) have been rare and, relative to other herbicide mode of action target-site mutations, unconventionally weak in magnitude for resistance to glyphosate. However, it is possible that weeds will emerge with non-synonymous mutations of two codons of EPSPS to produce an enzyme endowing greater resistance to glyphosate. Today, target-gene duplication is a common glyphosate resistance mechanism and could become a fundamental process for developing any resistance trait. Based on competition and substrate selectivity studies in several species, rapid vacuole sequestration of glyphosate occurs via a transporter mechanism. Conversely, as the chloroplast requires transporters for uptake of important metabolites, transporters associated with the two plastid membranes may separately, or together, successfully block glyphosate delivery. A model based on finite glyphosate dose and limiting time required for chloroplast loading sets the stage for understanding how uniquely different mechanisms can contribute to overall glyphosate resistance.

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Section: Gene Duplicationmentioning

confidence: 99%

Glyphosate resistance: state of knowledge

Sammons

Gaines

2014

Pest Management Science

400

609

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“…Several studies related to glyphosate resistance and elevated EPSPS copy number in Palmer amaranth and related species are available [18,22,31,42,43]. Elevated EPSPS copy number has also been identified as a glyphosate resistance mechanism in ryegrass [40].…”

Section: Discussionmentioning

confidence: 99%

Varying Tolerance to Glyphosate in a Population of Palmer Amaranth with Low EPSPS Gene Copy Number

Teaster¹,

Hoagland²

2013

AJPS

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A Palmer amaranth population (seeds collected in the year 2000; Washington Co., MS) suspected to be susceptible to glyphosate was examined as a population and as individual plants and found to exhibit varying tolerance or resistance to glyphosate. Whole plant spraying of glyphosate (0.84 kg·ha ) to the population revealed that approximately 40% of this population were resistant to glyphosate and an LD 50 of 0.75 kg·ha −1 was determined. Spray application of glyphosate indicated that some plants displayed varying degrees of resistance 14 days after treatment. Initial tests using leaf disc bioassays on 10 individual plants selected randomly from the population, allowed characterization of glyphosate resistance using both visual ratings of injury and quantitative measurement via chlorophyll content analysis. After initial bioassays and spray application, five plants with a range of tolerance to glyphosate were selected for cloning so that further studies could be accomplished on these individuals. Q-PCR analysis of these clones showed that resistance was not due to elevated EPSPS gene copy number. Shikimate levels were lower in the resistant and higher in the susceptible clones which correlated with varying degrees of resistance demonstrated in bioassays and spray application of glyphosate of these clones. Results demonstrate that individuals in a population can vary widely with respect to herbicide resistance and suggest that uptake, translocation, sequestration, metabolism or altered target site may contribute to the resistance in some individuals of this population.

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“…In these cases, the target-site mechanism of resistance detected in Eleusine indica and the selective sequestration of glyphosate into vacuoles (non-target site mechanism) observed in C. canadensis would be similarly inherited (Ng et al, 2004b;Ge et al, 2010). On the other hand, the variable number of EPSPS copies explains the different glyphosate sensitivities in resistant A. palmeri and could influence the type of glyphosate resistance inheritance, determining whether it is monogenic or polygenic (Chandi et al, 2012;Mohseni-Moghadam et al, 2013).…”

Section: Cross-breedingmentioning

confidence: 99%

“…Several authors found that resistance to glyphosate is controlled either by single genes with different levels of dominance (Ng et al, 2004a;Zelaya et al, 2004;Wakelin and Preston, 2006) or by multiple genes (Simarmata et al, 2005;Chandi et al, 2012). This information is particularly relevant in understanding and modelling the evolution of resistance (Gressel and Segel, 1978;Neve et al, 2011).…”

Section: Introductionmentioning

confidence: 99%