Location: Crop Production Systems ResearchTitle: Target site-based resistance to ALS inhibitors, glyphosate, and PPO inhibitors in an Amaranthus palmeri accession from Mississippi
|NANDULA, VIJAY - US Department Of Agriculture (USDA)|
|GIACOMINI, DARCI - University Of Illinois|
Submitted to: American Journal of Plant Sciences
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/8/2020
Publication Date: 8/11/2020
Citation: Nandula, V.K., Giacomini, D.A., Molin, W.T. 2020. Target site-based resistance to ALS inhibitors, glyphosate, and PPO inhibitors in an Amaranthus palmeri accession from Mississippi. American Journal of Plant Sciences. 11:1206-1216. https://doi.org/10.4236/ajps.2020.118085.
Interpretive Summary: Glyphosate resistant Palmer pigweed (Amaranthus palmeri), a highly competitive weed, has spread across the USA and has now been found to evolve resistance to two other herbicide classes. Scientists in the USDA-ARS Crop Production Systems Research Unit, Stoneville, MS and the University of Illinois conducted research to determine the basis for resistance to acetolactate inhibiting herbicides and protoporphyrinogen inhibiting herbicides. Point mutations were responsible for resistance to these new target sites resulting in multiple herbicide resistance in a single species. These results are important to farmers because it shows the necessity for increased diligence in herbicide use to prevent the development and spread of herbicide resistant weeds.
Technical Abstract: Widespread adoption of glyphosate-resistant (GR) crops and the associated use of glyphosate has resulted in evolution of GR weeds in several states of the US including Mississippi. GR Amaranthus palmeri populations are widespread across the state with some exhibiting multiple resistance to acetolactate synthase (ALS) inhibiting herbicides such as pyrithiobac. A GR and ALS inhibitor-resistant accession was also resistant to the protoporphyrinogen oxidase (PPO) inhibiting herbicide fomesafen. The PPO inhibitor resistance profile and multiple herbicide resistance mechanisms in this accession were investigated. In addition to fomesafen, resistance to postemergence applications of acifluorfen, lactofen, carfentrazone, and sulfentrazone was confirmed. There was no resistance to preemergence application of fomesafen, flumioxazin, or oxyfluorfen. Molecular analysis of the ALS gene indicated the presence of point mutations leading to single nucleotide substitutions at codons 197, 377, 574, and 653, resulting in proline-to-serine, arginine-to-glutamine, tryptophan-to-leucine, and serine-to-asparagine replacements, respectively. The resistant accession contained up to 87-fold more copies of the EPSPS gene compared to a susceptible accession. A mutation leading to a deletion of glycine at codon 210 ('G210) of PPO2 gene was also detected. These results indicate that the mechanism of resistance in the Palmer amaranth accession is target-site based, i.e., altered target site for ALS and PPO inhibitor resistance and gene amplification for glyphosate resistance.