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Herbicide metabolism and EPSPS Pro-106-Ser substitution confer multiple resistance in Chenopodium spp. from Southern Spain.

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Title: Herbicide metabolism and EPSPS Pro-106-Ser substitution confer multiple resistance in Chenopodium spp. from Southern Spain.
Authors: Rojano-Delgado, Antonia M.1 (AUTHOR), Sohrabi, Sima2 (AUTHOR), Santana, Ana Paula da Silva3 (AUTHOR), Palma-Bautista, Candelario4 (AUTHOR), Domínguez-Valenzuela, José Alfredo4 (AUTHOR), Gherekhloo, Javid5 (AUTHOR), Alcántara-de la Cruz, Ricardo1,3 (AUTHOR) ricardo.delacruz@ufv.br, De Prado, Rafael6 (AUTHOR)
Source: Pesticide Biochemistry & Physiology. Jun2026, Vol. 221, pN.PAG-N.PAG. 1p.
Subject Terms: *Herbicide resistance, *Glyphosate, Cytochrome P-450, Goosefoots
Geographic Terms: Spain, Southern Spain, Southern Europe
Abstract: Long-term herbicide programs in Mediterranean perennial systems have imposed sustained selection pressure on weed populations, promoting the evolution of multiple resistance. We investigated resistance mechanisms in Chenopodium album (Ca) and C. vulvaria (Cv) from southern Spain following more than two decades of glyphosate-based management. We aimed to (i) confirm resistance to atrazine, tribenuron-methyl (TM), glyphosate, and 2,4-D; (ii) distinguish between target-site and metabolic resistance; and (iii) characterize the biochemical and molecular basis of cross- and multiple-herbicide resistance. Screening assays revealed high survival (78–100%) of resistant (R) populations to acetolactate synthase (ALS)-, photosystem II (PSII)-, auxinic-, and 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS)-inhibiting herbicides. Dose–response assays confirmed resistance, with resistance indices (RI) of 6.7 and 5.1 for atrazine, 19.0 and 17.3 for TM, 7.0 and 13.9 for glyphosate, and 6.0 and 6.9 for 2,4-D in CaR and CvR, respectively. Radiolabelled and analytical metabolism assays demonstrated enhanced herbicide metabolism in R populations: atrazine (94–95% vs. 13–16% in S), TM (68–69% vs. 24–25%), 2,4-D (64–65% vs. 2–4%), and glyphosate (39–43% vs. 8–9%). Malathion partially reversed resistance to atrazine, TM, and 2,4-D, supporting cytochrome P450 (CYP450) involvement. In contrast, glyphosate metabolism was independent of CYP450 or glutathione S-transferases inhibition. Biochemical assays showed no differences in PSII or ALS sensitivity (I₅₀ RI ≈ 1), whereas EPSPS inhibition assays revealed a tenfold increase in I₅₀ in CvR. Sequencing identified a Pro-106-Ser substitution in EPSPS exclusively in CvR. Enhanced metabolism predominates in the R Chenopodium spp. populations, with coexistence of metabolic and target-site mechanisms in CvR, increasing the risk of further cross-resistance under continued herbicide reliance. [Display omitted] • Multiple resistance confirmed to PSII, ALS, EPSPS and auxinic herbicides. • CYP450-mediated metabolism contributes to atrazine, 2,4-D, and TM resistance. • Glyphosate resistance associated with metabolism of unknown basis. • EPSPS Pro-106-Ser mutation detected in resistant C. vulvaria. • Metabolic and target-site mechanisms coexist in CvR population. [ABSTRACT FROM AUTHOR]
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Description
Abstract:Long-term herbicide programs in Mediterranean perennial systems have imposed sustained selection pressure on weed populations, promoting the evolution of multiple resistance. We investigated resistance mechanisms in Chenopodium album (Ca) and C. vulvaria (Cv) from southern Spain following more than two decades of glyphosate-based management. We aimed to (i) confirm resistance to atrazine, tribenuron-methyl (TM), glyphosate, and 2,4-D; (ii) distinguish between target-site and metabolic resistance; and (iii) characterize the biochemical and molecular basis of cross- and multiple-herbicide resistance. Screening assays revealed high survival (78–100%) of resistant (R) populations to acetolactate synthase (ALS)-, photosystem II (PSII)-, auxinic-, and 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS)-inhibiting herbicides. Dose–response assays confirmed resistance, with resistance indices (RI) of 6.7 and 5.1 for atrazine, 19.0 and 17.3 for TM, 7.0 and 13.9 for glyphosate, and 6.0 and 6.9 for 2,4-D in CaR and CvR, respectively. Radiolabelled and analytical metabolism assays demonstrated enhanced herbicide metabolism in R populations: atrazine (94–95% vs. 13–16% in S), TM (68–69% vs. 24–25%), 2,4-D (64–65% vs. 2–4%), and glyphosate (39–43% vs. 8–9%). Malathion partially reversed resistance to atrazine, TM, and 2,4-D, supporting cytochrome P450 (CYP450) involvement. In contrast, glyphosate metabolism was independent of CYP450 or glutathione S-transferases inhibition. Biochemical assays showed no differences in PSII or ALS sensitivity (I₅₀ RI ≈ 1), whereas EPSPS inhibition assays revealed a tenfold increase in I₅₀ in CvR. Sequencing identified a Pro-106-Ser substitution in EPSPS exclusively in CvR. Enhanced metabolism predominates in the R Chenopodium spp. populations, with coexistence of metabolic and target-site mechanisms in CvR, increasing the risk of further cross-resistance under continued herbicide reliance. [Display omitted] • Multiple resistance confirmed to PSII, ALS, EPSPS and auxinic herbicides. • CYP450-mediated metabolism contributes to atrazine, 2,4-D, and TM resistance. • Glyphosate resistance associated with metabolism of unknown basis. • EPSPS Pro-106-Ser mutation detected in resistant C. vulvaria. • Metabolic and target-site mechanisms coexist in CvR population. [ABSTRACT FROM AUTHOR]
ISSN:00483575
DOI:10.1016/j.pestbp.2026.107132