Abstract
The foliar retention, absorption, translocation, and diffusion of glyphosate in glyphosate resistant-(R) and susceptible (S)-Palmer amaranth populations from seed collected in Georgia in 2007 were examined. The R population of Palmer amaranth had an elevated copy number of the EPSPS gene conferring the mechanism of resistance. When applications of 14C-glyphosate to a single leaf followed entire plant treatment with glyphosate, the distribution percentages were similar for R and S for the above and below treated leaves when harvested at 1, 6, 12, 24, and 48 hours after treatment (HAT). There were initially no differences between R and S at 1 HAT with an average of 8% absorption for both biotypes. However, data indicated that glyphosate absorption increased for R-Palmer amaranth reaching 41% within 6 HAT and was significantly different (P = 0.01) from the 28% absorbed by S-Palmer amaranth. Glyphosate resistant and susceptible Palmer amaranth averaged 44% 14C-glyphosate absorption by 24 HAT. There were no differences for 14C-glyphosate Bq/mg of plant tissue between R and S for the above the treated leaf and below the treated leaf portions of plants at 1, 6, 12, 24, or 48 HAT. However, root accumulation of 14C-glyphosate in plant tissue was significantly greater by 12 HAT for the roots of R (1.21 Bq/mg) than for S (0.51 Bq/mg). The treated leaf of the R-Palmer amaranth plants exhibited greater translocation of 14C-glyphosate in Bq/mg of tissue than the susceptible over time, indicating no detrimental effect or cost of fitness due to EPSPS gene amplification. Additionally, there were no differences in glyphosate retention in leaf discs assays between R and S biotypes. In spite of an average of 6.5 Bq efflux out of R and S leaf discs after 15 minute, only 0.4 Bq was retained after 150 minutes. Glyphosate was not retained over time in the leaf discs for R and S, and there were no biotype differences within bathing times. However, the rate of efflux (the slope of the curves) was greater for the R biotype. These data support the reported gene amplification non-target site glyphosate resistance mechanism in Palmer amaranth.
Highlights
The use of glyphosate as a tool for weed control has become a standard practice for large scale glyphosate resistant crop production and vegetation management around the world
The data presented in this study support previous research demonstrating that the glyphosate resistance mechanism in Palmer Amaranth is gene amplification of 5-eno-pysuvylshikimate-2-phosphate synthase [2] [13] [14]
With enol-pyruvylshikimate-3phosphate synthase (EPSPS) gene amplification, the wildtype form of EPSPS is inhibited by glyphosate so if enough is applied, some level of control will be achieved [2]
Summary
The use of glyphosate as a tool for weed control has become a standard practice for large scale glyphosate resistant crop production and vegetation management around the world. The extensive application of glyphosate for glyphosate-resistant crop weed control promoted selection pressure for the occurrence of glyphosate-resistant (R) Palmer amaranth to appear in Georgia in 2004 [2], [3], subsequently occurring throughout the Southern United States [4]. It became the most troublesome weed of cotton in the region by 2009 [5] and 2013 [6]. The mechanism of resistance is novel and attributed to increased copies of the gene required for production of the enzyme 5-enol-pyruvylshikimate-3phosphate synthase (EPSPS), with reports of up to 100 copies occurring in this population of R-Palmer amaranth [7]
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