Affiliation:
1. Department of Agricultural and Forest Sciences and Engineering University of Lleida – Agrotecnio CERCA Center Lleida Spain
2. Departmento de Agronomia Universidade Federal de Viçosa Viçosa Brazil
3. Department of Agricultural Biology Colorado State University Fort Collins CO USA
4. Department of Agronomy Kansas State University Manhattan KS USA
5. Department of Crop Science Federal University of Rio Grande do Sul Porto Alegre Brazil
6. Departamento de Parasitología Agrícola Universidad Autónoma Chapingo Texcoco Mexico
7. Department of Agricultural Chemistry and Soil Science University of Córdoba Córdoba Spain
8. Department of Crop Sciences University of Illinois at Urbana‐Champaign Urbana IL USA
Abstract
AbstractThe commercialization of 2,4‐D (2,4‐dichlorophenoxyacetic acid) latifolicide in 1945 marked the beginning of the selective herbicide market, with this active ingredient playing a pivotal role among commercial herbicides due to the natural tolerance of monocots compared with dicots. Due to its intricate mode of action, involving interactions within endogenous auxin signaling networks, 2,4‐D was initially considered a low‐risk herbicide to evolve weed resistance. However, the intensification of 2,4‐D use has contributed to the emergence of 2,4‐D‐resistant broadleaf weeds, challenging earlier beliefs. This review explores 2,4‐D tolerance in crops and evolved resistance in weeds, emphasizing an in‐depth understanding of 2,4‐D metabolic detoxification. Nine confirmed 2,4‐D‐resistant weed species, driven by rapid metabolism, highlight cytochrome P450 monooxygenases in Phase I and glycosyltransferases in Phase II as key enzymes. Resistance to 2,4‐D may also involve impaired translocation associated with mutations in auxin/indole‐3‐acetic acid (Aux/IAA) co‐receptor genes. Moreover, temperature variations affect 2,4‐D efficacy, with high temperatures increasing herbicide metabolism rates and reducing weed control, while drought stress did not affect 2,4‐D efficacy. Research on 2,4‐D resistance has primarily focused on non‐target‐site resistance (NTSR) mechanisms, including 2,4‐D metabolic detoxification, with limited exploration of the inheritance and genetic basis underlying these traits. Resistance to 2,4‐D in weeds is typically governed by a single gene, either dominant or incompletely dominant, raising questions about gain‐of‐function or loss‐of‐function mutations that confer resistance. Future research should unravel the physiological and molecular‐genetic basis of 2,4‐D NTSR, exploring potential cross‐resistance patterns and assessing fitness costs that may affect future evolution of auxin‐resistant weeds. © 2024 Society of Chemical Industry.