Filipi Mesquita Machado

Herbicide target site resistance in polyploid species is more complex than in diploids due to potential subgenome interactions. This study characterized mutations in the ALS gene across distinct subgenomes of hexaploid Echinochloa crus‐galli and evaluated the cross‐resistance patterns conferred by each mutation to various ALS‐inhibiting herbicides. E. crus‐galli populations were screened, and dose–response curves were performed with ALS inhibitors from different chemical groups. The ALS gene copies of each subgenome (A, B, and C) were sequenced. Copy number variation, global relative expression, and the specific relative expression of ALS gene from each subgenome were performed. The mutations Ala122Thr, Ala205Asn, and Ser653Asn conferred resistance only to imazethapyr, whereas Trp574Leu to imazethapyr, penoxsulam, bispyribac‐sodium, and nicosulfuron, when considered the label rate. ALS mutations were more frequent in subgenome A, but ALS from subgenome C had the highest expression. Biotypes with the same mutation showed different resistance level to herbicides. The biotype SAOJER‐01 had Trp574Leu mutation in subgenome C and was 22 times more resistant to imazethapyr and penoxsulam than CAMAQ‐01, which had the same Trp574Leu mutation in subgenome A. Both SAOJER‐01 and CAMAQ‐01 biotypes showed CYP450 metabolism mediating penoxsulam resistance in addition to the target site mutation. In conclusion, the mutations Ala122Thr, Ala205Asn, Trp574Leu, and Ser653Asn confer resistance to imazethapyr, but only Trp574Leu confers resistance to the other chemical groups. The herbicides penoxsulam, bispyribac‐sodium, and nicosulfuron are effective in controlling three out of four mutations. CYP450‐mediated metabolism coexists in biotypes carrying the Trp574Leu mutation. The subgenome location of the ALS mutation may result in variable levels of resistance.

Herbicide target site resistance in polyploid species is more complex than diploids due to potential subgenome interactions and gene dosage of mutations. The objective of this study was to identify the level of resistance and cross-resistance patterns of ALS mutations located in the different subgenomes of allohexaploid Echinochloa crus-galli . E. crus-galli populations were screened and dose-response curves were performed with ALS-inhibitors from different chemical groups. The ALS genes of each subgenome (A, B, and C) were sequenced. Copy number variation, global relative expression, and the specific relative expression of ALS gene from each subgenome were performed. Out of 100 populations, 32% were resistant only to imazethapyr, and 48% were cross-resistant to all ALS-inhibitors. The mutations Ala122Thr, Ala205Asn, and Ser653Asn confer resistance only to imazethapyr, while Trp574Leu confers resistance to all four herbicides tested. ALS mutations were most frequent in subgenome A, but ALS from subgenome C had the highest expression. The biotype SAOJER-01 had Trp574Leu mutation in subgenome C and was 22 times more resistant to imazethapyr and penoxsulam than CAMAQ-01, which had the same Trp574Leu mutation in subgenome A with no differences in herbicide metabolism rate. The ALS genes from subgenomes A and C contribute approximately 13% and 50% respectively to the total ALS transcripts. The higher contribution of subgenome C to the total ALS transcripts pool combined with the Trp574Leu resistance mutation makes the biotype SAOJER-01 more resistant to herbicides than CAMAQ-01. This is the first study showing the effect of subgenome gene expression level on the herbicide resistance level in a polyploid weed species. In addition, while imazethapyr did not control any biotype with an ALS mutation, the other ALS-inhibitor herbicides were able to control biotypes carrying Ala122Thr, Ala205Asn, and Ser653Asn, which reinforces the utility of these herbicides in weed and resistance management.

BACKGROUND: Amaranthus tuberculatus (Moq.) Sauer (waterhemp) has emerged as one of several weed species that is resistant to synthetic auxin herbicides (SAHs). Among the mechanisms of resistance to SAHs, nontarget‐site resistance (NTSR) has been of particular concern owing to its complexity. Here, we integrated linkage mapping with transcriptome analysis to explore NTSR mechanisms to two SAHs, dicamba and 2,4‐D, in a multiple‐herbicide‐resistant A. tuberculatus population (CHR).RESULTS: Phenotypic evaluations of an F₂ mapping population indicated a polygenic basis for both dicamba and 2,4‐D resistance in CHR. A weak correlation was observed between phenotypic responses to dicamba and 2,4‐D treatments. Linkage mapping analyses revealed eight quantitative trait loci (QTL) regions associated with dicamba and 2,4‐D resistance mapped to seven A. tuberculatus chromosomes. Together, these QTL regions explained 24.2 and 23.1% of the variation in dicamba‐ and 2,4‐D‐resistant phenotypes, respectively. Only one co‐localized QTL region was found between the two resistance traits.CONCLUSION: The results of this study demonstrated that resistance to dicamba and 2,4‐D in the CHR population is under the control of genes at multiple loci. The weak phenotypic and genetic associations of resistance traits indicate that more than one NTSR mechanism confers resistance to dicamba and 2,4‐D in this A. tuberculatus population. © 2025 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

BACKGROUND: Giant ragweed (Ambrosia trifida L.) is one of the most troublesome weed species in corn (Zea mays L.) and soybean [Glycine max (L.) Merr.] cropping systems. Following numerous reports in 2018 of suspected herbicide resistance in several Ambrosia trifida populations from Wisconsin, our objective was to characterize the response of these accessions to acetolactate synthase (ALS), enolpyruvyl shikimate phosphate synthase (EPSPS), and protoporphyrinogen oxidase (PPO) inhibitors applied POST.RESULTS: Four accessions (AT1, AT4, AT6, and AT10) exhibited ≥ 50% plant survival after exposure to the cloransulam 3× rate. Two accessions (AT8 and AT10) and one accession (AT2) exhibited ≥ 50% plant survival after exposure to glyphosate and fomesafen 1× rates, respectively. The AT10 accession exhibited multiple resistance to cloransulam and glyphosate. The AT12 accession was 28.8‐fold resistant to fomesafen and 3.7‐fold resistant to lactofen. A codon change in PPX2 conferring a R98L substitution was identified as the most likely mechanism conferring PPO‐inhibitor resistance.CONCLUSION: To our knowledge, this is the first confirmed case of PPO‐inhibitor resistance in Ambrosia trifida globally and we identified the genetic mutation likely conferring resistance. Proactive and diversified integrated weed management strategies are of paramount importance for sustainable long‐term Ambrosia trifida management. © 2024 The Author(s). Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Resistant plants of Sumatran fleabane with unusual rapid necrosis (RN) symptoms after application of 2,4-D were characterized in previous studies. Field observations indicated variability in the occurrence of the RN caused by 2,4-D, but the causes of the variation are unknown. This study aimed to investigate the effect of environmental conditions, plant growth stage, and simultaneous and sequential herbicide mixtures with other auxin mimics on the occurrence of RN caused by 2,4-D. Application at temperature of 12 C delayed the symptoms and decreased the intensity of the RN but still resulted in plant survival to 2,4-D. The absence of light after herbicide application caused a slight delay in the symptoms, but the production of hydrogen peroxide and the size of the necrosed area were not affected by the light treatments before and after 2,4-D application. Changes in plant photosynthesis through inhibiting photosystem II do not prevent the occurrence of RN symptoms. The auxinic herbicides dicamba, triclopyr, and halauxifen-methyl do not cause RN symptoms and are effective at controlling the resistant biotype when applied without 2,4-D, but the effectiveness of these herbicides was reduced when sprayed on the resistant biotype either together, 4 h, or 24 h after 2,4-D. The RN phenotype does not occur for dicamba and triclopyr, even in advanced plant growth stages and high doses on the resistant biotype. The herbicides dicamba and triclopyr effectively controlled resistant plants, especially when sprayed at the initial growth stages. The results of this study identify environmental effects, plant development effects, and herbicide interactions that interfere with the occurrence of RN symptoms caused by 2,4-D in Sumatran fleabane. These data provide insights about the mechanisms behind the RN symptoms caused by 2,4-D and are important for identifying the causes of variability of the herbicide symptomology and performance under experimental and field conditions.