1. Confirmation and inheritance of glufosinate resistance in an Amaranthus palmeri population from North Carolina
- Author
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Eric A. L. Jones, Jeffrey C. Dunne, Charles W. Cahoon, Katherine M. Jennings, Ramon G. Leon, and Wesley J. Everman
- Subjects
glufosinate ,herbicide resistance ,inheritance ,oligogenic ,Environmental sciences ,GE1-350 ,Botany ,QK1-989 - Abstract
Abstract A putative glufosinate‐resistant Amaranthus palmeri population was reported in 2015 in Anson County, North Carolina. The results from dose–response assays conducted in the field suggested plants were surviving lethal rates of glufosinate. Dose–response assays conducted in the glasshouse determined the Anson County accession exhibited reduced susceptibility to glufosinate compared to three glufosinate‐susceptible populations. The LD50 values (210–316 g ai ha−1) for the Anson County population were always higher than the LD50 values (118–158 g ai ha−1) for the tested susceptible populations from the dose–response assays. Anson County plants that survived lethal glufosinate rates were reciprocally crossed with susceptible plants to create F1 genotypes and treated with a lethal rate of glufosinate (267 g ai ha−1; ascertained from glasshouse dose–response assay) to determine the distribution of injury and survival for each cross compared to a cross of susceptible parents. The distribution of injury was non‐normal for the crosses containing an Anson County plant compared to the cross with a susceptible parent. Survival was 68%–84% for crosses containing an Anson County plant, whereas the survival was significantly reduced to 35% for the susceptible plant cross. Chi‐square goodness of fit tests were used to test inheritance models to describe the responses of the genotypes. The resistant × susceptible crosses were best described with a heterozygous two loci with incomplete dominance model compared to the resistant × resistant cross that was best described with a heterozygous single locus with incomplete dominance model. The Anson County population has evolved resistance to glufosinate that is heritable and likely conferred by an oligogenic mechanism with incomplete dominance.
- Published
- 2024
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