Resistance to acetyl‐CoA carboxylase‐inhibiting herbicides

Abstract

Resistance to acetyl-CoA carboxylase herbicides is documented in at least 43 grass weeds and is particularly problematic in Lolium, Alopecurus and Avena species. Genetic studies have shown that resistance generally evolves independently and can be conferred by target-site mutations at ACCase codon positions 1781, 1999, 2027, 2041, 2078, 2088 and 2096. The level of resistance depends on the herbicides, recommended field rates, weed species, plant growth stages, specific amino acid changes and the number of gene copies and mutant ACCase alleles. Non-target-site resistance, or in essence metabolic resistance, is prevalent, multigenic and favoured under low-dose selection. Metabolic resistance can be specific but also broad, affecting other modes of action. Some target-site and metabolic-resistant biotypes are characterised by a fitness penalty. However, the significance for resistance regression in the absence of ACCase herbicides is yet to be determined over a practical timeframe. More recently, a fitness benefit has been reported in some populations containing the I1781L mutation in terms of vegetative and reproductive outputs and delayed germination. Several DNA-based methods have been developed to detect known ACCase resistance mutations, unlike metabolic resistance, as the genes remain elusive to date. Therefore, confirmation of resistance is still carried out via whole-plant herbicide bioassays. A growing number of monocotyledonous crops have been engineered to resist ACCase herbicides, thus increasing the options for grass weed control. While the science of ACCase herbicide resistance has progressed significantly over the past 10 years, several avenues provided in the present review remain to be explored for a better understanding of resistance to this important mode of action.

Evolution, growth and phenology of Phalaris minor biotypes resistant to ACCase-inhibiting herbicides in Mexico

“…A similar result in the ACCase gene has been documented by Délye (2005). Further, all mutations found in samples from the "El Bajio" region have been reported previously by Kaundun (2014) in grasses. For example, in the Gto biotype, a mutation in position 1,781 (Ile x Leu) was found and it has been reported to confer resistance to three chemical families (aryloxyphenoxypropionate, cyclohexanedione and phenylpyrazoline) (Powles & Yu 2010).…”

Analysis of Arabidopsis Accessions Hypersensitive to a Loss of Chloroplast Translation

“…Several common herbicides target the plastid-localized homomeric enzyme in grasses while not interfering with the cytosolic or heteromeric enzymes found elsewhere. Resistant plants have alterations in one of seven residues located within the carboxyltransferase-binding domain (Zhang et al, 2004;Liu et al, 2007;Kaundun, 2014). The cytosolic ACC1 protein in Arabidopsis enables the biosynthesis of very-long-chain fatty acids (Baud et al, 2004;Lü et al, 2011;Amid et al, 2012), which function in plant protection and signaling pathways and limit the regeneration capacity of roots (Shang et al, 2016).…”

“…This work provides valuable insights into essential domains within a large, homodimeric enzyme that represents a target for herbicide action (Kaundun, 2014) and pharmaceuticals for human diseases (Harriman et al, 2016). Identification of Arabidopsis accessions hypersensitive to spectinomycin should also advance research on chloroplast transformation, where spectinomycin is the selection agent of choice (Svab and Maliga, 1993), and may help to uncover a novel function for ACC2 in some Arabidopsis populations.…”

Weed Control and Selectivity to Post-Applied Herbicides in Eucalyptus

“…At the cellular level, these graminicides block the biosynthesis of fatty acids, making it impossible to form lipids and, consequently, affecting the integrity of the cell membrane. Thus, the extravasation of the intracellular contents occurs, leading to the death of the cells of the growth tissues (Délye, 2005;Kaundun, 2014). Johnson & Hoverstad, 2002).…”