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Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype
Euphorbia heterophylla is a weed species that invades extensive crop areas in subtropical regions of Brazil. This species was previously controlled by imazamox, but the continuous use of this herbicide has selected for resistant biotypes. Two biotypes of E. heterophylla from southern Brazil, one res...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6817884/ https://www.ncbi.nlm.nih.gov/pubmed/31659241 http://dx.doi.org/10.1038/s41598-019-51682-z |
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author | Rojano-Delgado, Antonia M. Portugal, João M. Palma-Bautista, Candelario Alcántara-de la Cruz, Ricardo Torra, Joel Alcántara, Esteban De Prado, Rafael |
author_facet | Rojano-Delgado, Antonia M. Portugal, João M. Palma-Bautista, Candelario Alcántara-de la Cruz, Ricardo Torra, Joel Alcántara, Esteban De Prado, Rafael |
author_sort | Rojano-Delgado, Antonia M. |
collection | PubMed |
description | Euphorbia heterophylla is a weed species that invades extensive crop areas in subtropical regions of Brazil. This species was previously controlled by imazamox, but the continuous use of this herbicide has selected for resistant biotypes. Two biotypes of E. heterophylla from southern Brazil, one resistant (R) and one susceptible (S) to imazamox, were compared. The resistance of the R biotype was confirmed by dose-response assays since it required 1250.2 g ai ha(−1) to reduce the fresh weight by 50% versus 7.4 g ai ha(−1) for the S biotype. The acetolactate synthase (ALS) enzyme activity was studied using ALS-inhibiting herbicides from five different chemical families. The R biotype required the highest concentrations to reduce this enzyme activity by 50%. A Ser653Asn mutation was found in the ALS gene of the R biotype. The experiments carried out showed that imazamox absorption and metabolism were not involved in resistance. However, greater (14)C-imazamox root exudation was found in the R biotype (~70% of the total absorbed imazamox). Target site mutation in the ALS gene is the principal mechanism that explains the imazamox resistance of the R biotype, but root exudation seems to also contribute to the resistance of this biotype. |
format | Online Article Text |
id | pubmed-6817884 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-68178842019-11-01 Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype Rojano-Delgado, Antonia M. Portugal, João M. Palma-Bautista, Candelario Alcántara-de la Cruz, Ricardo Torra, Joel Alcántara, Esteban De Prado, Rafael Sci Rep Article Euphorbia heterophylla is a weed species that invades extensive crop areas in subtropical regions of Brazil. This species was previously controlled by imazamox, but the continuous use of this herbicide has selected for resistant biotypes. Two biotypes of E. heterophylla from southern Brazil, one resistant (R) and one susceptible (S) to imazamox, were compared. The resistance of the R biotype was confirmed by dose-response assays since it required 1250.2 g ai ha(−1) to reduce the fresh weight by 50% versus 7.4 g ai ha(−1) for the S biotype. The acetolactate synthase (ALS) enzyme activity was studied using ALS-inhibiting herbicides from five different chemical families. The R biotype required the highest concentrations to reduce this enzyme activity by 50%. A Ser653Asn mutation was found in the ALS gene of the R biotype. The experiments carried out showed that imazamox absorption and metabolism were not involved in resistance. However, greater (14)C-imazamox root exudation was found in the R biotype (~70% of the total absorbed imazamox). Target site mutation in the ALS gene is the principal mechanism that explains the imazamox resistance of the R biotype, but root exudation seems to also contribute to the resistance of this biotype. Nature Publishing Group UK 2019-10-28 /pmc/articles/PMC6817884/ /pubmed/31659241 http://dx.doi.org/10.1038/s41598-019-51682-z Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Rojano-Delgado, Antonia M. Portugal, João M. Palma-Bautista, Candelario Alcántara-de la Cruz, Ricardo Torra, Joel Alcántara, Esteban De Prado, Rafael Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype |
title | Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype |
title_full | Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype |
title_fullStr | Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype |
title_full_unstemmed | Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype |
title_short | Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype |
title_sort | target site as the main mechanism of resistance to imazamox in a euphorbia heterophylla biotype |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6817884/ https://www.ncbi.nlm.nih.gov/pubmed/31659241 http://dx.doi.org/10.1038/s41598-019-51682-z |
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