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BACKGROUND: 2,4-Dichlorophenoxyacetic acid (2,4-D) and other auxinic herbicides are important for weed control in cropping systems globally. Weeds with resistance to 2,4-D and other auxinic herbicides have evolved, including several populations of Sonchus oleraceus from multiple sites in Australia. We report the underlying mechanism in these populations that gives rise to auxinic herbicide resistance. RESULTS: We studied a total of three susceptible and eight resistant Sonchus oleraceus populations. All resistant populations had a deletion of three amino acids flanking the degron sequence of an Aux/IAA gene, SoIAA20, which was not found in the three susceptible populations. The eight populations with the resistant allele were also resistant to dicamba, fluroxypyr and clopyralid. The resistant plants also had reduced movement of 2,4-D out of the treated tissues compared to susceptible plants. CONCLUSION: The paired deletion flanking the degron region of SoIAA20 likely provides resistance to 2,4-D by restricting the movement of 2,4-D from the treated tissue to the rest of the plant. We hypothesise that this deletion keeps the 2,4-D bound to the target site. © 2024 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
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BACKGROUND: Chloris virgata is a warm-season, C4 , annual grass weed affecting field crops in northern Australia that has become an emerging weed in southern Australia. Four populations with suspected resistance to glyphosate were collected in South Australia, Queensland and New South Wales, Australia, and compared with one susceptible (S) population to confirm glyphosate resistance and elucidate possible mechanisms of resistance. RESULTS: Based on the rate of glyphosate required to kill 50% of treated plants (LD50 ), glyphosate resistance (GR) was confirmed in four populations of C. virgata (V12, V14.2, V14.16 and V15). GR plants were 2-9.7-fold more resistant and accumulated less shikimate after glyphosate treatment than S plants. GR and S plants did not differ in glyphosate absorption and translocation. Target-site EPSPS mutations corresponding to Pro-106-Leu (V14.2) and Pro-106-Ser (V15, V14.16 and V12) substitutions were found in GR populations. The population with Pro-106-Leu substitution was 2.9-4.9-fold more resistant than the three other populations with Pro-106-Ser substitution. CONCLUSION: This report confirms glyphosate resistance in C. virgata and shows that target-site EPSPS mutations confer resistance to glyphosate in this species. The evolution of glyphosate resistance in C. virgata highlights the need to identify alternative control tactics. © 2016 Society of Chemical Industry.
Asunto(s)
Glicina/análogos & derivados , Resistencia a los Herbicidas/genética , Herbicidas/farmacología , Mutación , Poaceae/genética , 3-Fosfoshikimato 1-Carboxiviniltransferasa/genética , Australia , Glicina/farmacología , Proteínas de Plantas/genética , Poaceae/efectos de los fármacos , Poaceae/fisiología , GlifosatoRESUMEN
BACKGROUND: Two oriental mustard populations (P2 and P13) collected from Port Broughton, South Australia were identified as resistant to 2,4-D. The level of resistance, mechanism and the mode of inheritance for 2,4-D resistance in these populations were investigated. RESULTS: Populations P2 and P13 were confirmed to be resistant to 2,4-D at the field rate (600 g a.e. ha-1 ). P2 and P13 were 81- and 67-fold more resistant than the susceptible populations (S1 and S2) at the dose required for 50% mortality (LD50 ), respectively. No predicted amino acid modification was detected in sequences of potential target-site genes (ABP, TIR1 and AFB5). Resistant populations had reduced 2,4-D translocation compared with the susceptible populations, with 77% of [14 C]2,4-D retained in the treated leaf versus 32% at 72 h after treatment. Resistance to 2,4-D is encoded on the nuclear genome and is dominant, as the response to 2,4-D of all F2 individuals were similar to the resistant biotypes. The segregation of F2 phenotypes fitted a 3: 1 (R: S) inheritance model. CONCLUSION: Resistance to 2,4-D in oriental mustard is likely due to reduced translocation of 2,4-D out of the treated leaf. Inheritance of 2,4-D resistance is conferred by a single gene with a high level of dominance. © 2017 Society of Chemical Industry.
Asunto(s)
Ácido 2,4-Diclorofenoxiacético/farmacología , Brassicaceae/efectos de los fármacos , Resistencia a los Herbicidas/genética , Herbicidas/farmacología , Brassicaceae/genética , Herencia , Mutación , Hojas de la Planta/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Australia del SurRESUMEN
Bread wheat (Triticum aestivum L.) has a major salt tolerance locus, Kna1, responsible for the maintenance of a high cytosolic K(+) /Na(+) ratio in the leaves of salt stressed plants. The Kna1 locus encompasses a large DNA fragment, the distal 14% of chromosome 4DL. Limited recombination has been observed at this locus making it difficult to map genetically and identify the causal gene. Here, we decipher the function of TaHKT1;5-D, a candidate gene underlying the Kna1 locus. Transport studies using the heterologous expression systems Saccharomyces cerevisiae and Xenopus laevis oocytes indicated that TaHKT1;5-D is a Na(+) -selective transporter. Transient expression in Arabidopsis thaliana mesophyll protoplasts and in situ polymerase chain reaction indicated that TaHKT1;5-D is localised on the plasma membrane in the wheat root stele. RNA interference-induced silencing decreased the expression of TaHKT1;5-D in transgenic bread wheat lines which led to an increase in the Na(+) concentration in the leaves. This indicates that TaHKT1;5-D retrieves Na(+) from the xylem vessels in the root and has an important role in restricting the transport of Na(+) from the root to the leaves in bread wheat. Thus, TaHKT1;5-D confers the essential salinity tolerance mechanism in bread wheat associated with the Kna1 locus via shoot Na(+) exclusion and is critical in maintaining a high K(+) /Na(+) ratio in the leaves. These findings show there is potential to increase the salinity tolerance of bread wheat by manipulation of HKT1;5 genes.