Abstract
Herbicides play an important role in preventing crop yield losses due to both their weed interference ability and their capacity for increasing soil conservation in no-till systems. Group A herbicides or acetyl-CoA carboxylase (ACCase) are essential tools the selective management of glyphosate resistance in grass weed species. In this review, we describe important aspects of ACCase biology and herbicides targeting this enzyme, along with a discussion on stewardship programs to delay the evolution of herbicide resistance which can evolve either through target site and/or non-target site mechanisms. Sixteen-point mutations have been reported to confer resistance to ACCase inhibitors. Each mutation confers cross resistance to a different group of herbicides. Metabolic resistance can result in resistance to multiple herbicides with different mechanisms of action (MoA), and herbicide detoxification is often conferred by cytochrome P450 monooxigenases and glutathione- S -transferases. Regardless of whether resistance mechanisms are target or non-target site, using herbicides with the same MoA will result in resistance evolution. Therefore, while field surveys and resistance mechanism studies are crucial for designing reactive management strategies, integrated weed management plays a central role in both reactive and proactive mitigation of herbicide resistance evolution.
Highlights
The world population has grown over the past few decades and is estimated to reach 9.7 billion people in 2050 (Gerland et al, 2014)
We describe important aspects of acetyl-CoA carboxylase (ACCase) biology and herbicides targeting this enzyme, along with a discussion on stewardship programs to delay the evolution of herbicide resistance which can evolve either through target site and/or non-target site mechanisms
Metabolic resistance can result in resistance to multiple herbicides with different mechanisms of action (MoA), and herbicide detoxification is often conferred by cytochrome P450 monooxigenases and glutathione-Stransferases
Summary
The world population has grown over the past few decades and is estimated to reach 9.7 billion people in 2050 (Gerland et al, 2014). Exceptions include susceptible Geraniaceae species and a few Brassica and Arabidopsis species (Kaundun, 2014) expressing the homomeric ACCase in their chloroplasts These herbicides halt ACCase activity by blocking fatty acid biosynthesis, preventing the formation of lipid and secondary metabolites in susceptible plants. Studies with pinoxaden showed this molecule has a very similar binding site to tepraloxydim, a DIM herbicide, despite considerable differences in their chemical structures (Yu et al, 2010; Kaundun, 2014) Do these findings suggest the wide variety of molecular mechanisms that underlie CT domain inhibition, and shed light on the importance of elucidating the molecular basis for target and crossresistance among ACCase-inhibiting herbicides (Xia et al, 2016)
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