Synthetic auxin herbicides: finding the lock and key to weed resistance

• Published in: Plant science (Limerick) 2020-11, Vol.300, p.110631, Article 110631
• Main Authors: Todd, Olivia E., Figueiredo, Marcelo R.A., Morran, Sarah, Soni, Neeta, Preston, Christopher, Kubeš, Martin F., Napier, Richard, Gaines, Todd A.
• Format: Article
• Language: English
• Subjects: 2,4-D; Aux/IAA; dicamba; Gene Expression Regulation, Plant; herbicide metabolism; herbicide resistance; Herbicide Resistance - genetics; Herbicide Resistance - physiology; Herbicides - metabolism; Indoleacetic Acids - metabolism; Plant Growth Regulators - metabolism; Plant Weeds - drug effects; Signal Transduction - genetics; Weed Control
• ISSN: 0168-9452; 1873-2259
• DOI: 10.1016/j.plantsci.2020.110631

•We explore known and hypothetical molecular resistance mechanisms for synthetic auxin herbicides.•Target site resistance for synthetic auxin herbicides occurs in the SCFTIR1/AFB ubiquitination complex and Aux/IAA co-receptors.•Enhanced metabolism mediated by cytochrome P450 s is key non-target-site resistance mechanism.•More research into synthetic auxin herbicide/target site interactions is needed.•Gene knockout mutations found in model plants for auxin insensitivity have not been found in weeds, possibly due to fitness costs for loss of function. Synthetic auxin herbicides are designed to mimic indole-3-acetic acid (IAA), an integral plant hormone affecting cell growth, development, and tropism. In this review, we explore target site genes in the auxin signaling pathway including SCFTIR1/AFB, Aux/IAA, and ARFs that are confirmed or proposed mechanisms for weed resistance to synthetic auxin herbicides. Resistance to auxin herbicides by metabolism, either by enhanced cytochrome P450 detoxification or by loss of pro-herbicide activation, is a major non-target-site resistance pathway. We speculate about potential fitness costs of resistance due to effects of resistance-conferring mutations, provide insight into the role of polyploidy in synthetic auxin resistance evolution, and address the genetic resources available for weeds. This knowledge will be the key to unlock the long-standing questions as to which components of the auxin signaling pathway are most likely to have a role in resistance evolution. We propose that an ambitious research effort into synthetic auxin herbicide/target site interactions is needed to 1) explain why some synthetic auxin chemical families have activity on certain dicot plant families but not others and 2) fully elucidate target-site cross-resistance patterns among synthetic auxin chemical families to guide best practices for resistance management.