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The 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. [ABSTRACT FROM AUTHOR]

Background: Resistance to 2,4‐Dichlorophenoxyacetic acid (2,4‐D) has been reported in several weed species since the 1950s; however, a biotype of Conyza sumatrensis showing a novel physiology of the rapid response minutes after herbicide application was reported in 2017. The objective of this research was to investigate the mechanisms of resistance and identify transcripts associated with the rapid physiological response of C. sumatrensis to 2,4‐D herbicide. Results: Differences were found in 2,4‐D absorption between the resistant and susceptible biotypes. Herbicide translocation was reduced in the resistant biotype compared to the susceptible. In resistant plants 98.8% of [14C] 2,4‐D was found in the treated leaf, whereas ≈13% translocated to other plant parts in the susceptible biotype at 96 h after treatment. Resistant plants did not metabolize [14C] 2,4‐D and had only intact [14C] 2,4‐D at 96 h after application, whereas susceptible plants metabolized [14C] 2,4‐D into four detected metabolites, consistent with reversible conjugation metabolites found in other 2,4‐D sensitive plant species. Pre‐treatment with the cytochrome P450 inhibitor malathion did not enhance 2,4‐D sensitivity in either biotype. Following treatment with 2,4‐D, resistant plants showed increased expression of transcripts within plant defense response and hypersensitivity pathways, whereas both sensitive and resistant plants showed increased expression of auxin‐response transcripts. Conclusion: Our results demonstrate that reduced 2,4‐D translocation contributes to resistance in the C. sumatrensis biotype. The reduction in 2,4‐D transport is likely to be a consequence of the rapid physiological response to 2,4‐D in resistant C. sumatrensis. Resistant plants had increased expression of auxin‐responsive transcripts, indicating that a target‐site mechanism is unlikely. © 2023 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]