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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., (© 2024 Society of Chemical Industry.)

Background: Conventional crossing of soft wheat cultivars resistant to imazamox and glufosinate resulted in two (Rados and Helter) lines resistant to both herbicides. Stacked traits conferring this dual herbicide resistance in these lines, compared with a susceptible (S) cultivar, were characterized., Results: Rados and Helter lines were ∼ 18-fold more resistant (R) to glufosinate, and between 15.1 and 19.8-fold more resistant to imazamox than the S cultivar. Resistance to glufosinate and imazamox decreased up to 12% and 50%, respectively, when the herbicides were applied sequentially. The basal activities of the acetolactate and glutamine synthases were similar between R and S plants. Rados and Helter lines were 11.7- and 17.7-fold more resistant to imazamox than the S cultivar, due to the Ser653-Asn mutation in their imi-ALS genes. R lines, susceptible to glufosinate at the target site level, showed lower ammonia accumulation evidencing the activity of the phosphinothricin acetyl transferase. Absorption and translocation patterns for 14 C-imazamox and 14 C-glufosinate were similar between R and S cultivars and so do not contribute to resistance., Conclusion: Stacked traits conferring dual herbicide resistance to the lines Rados and Helter come from the resistant parents. These R lines are potential tools for weed management in wheat production, mainly via herbicide rotation. © 2018 Society of Chemical Industry., (© 2018 Society of Chemical Industry.)