Target site as the main mechanism of resistance to imazamox in a Euphorbia heterophylla biotype release_ufysbirmmnevnarnbtb26rh7gy

by Antonia M. Rojano-Delgado, João M. Portugal, Candelario Palma-Bautista, Ricardo Alcántara-de la Cruz, Joel Torra, Esteban Alcántara, Rafael A. de Prado Amián

Published in Scientific Reports by Springer Science and Business Media LLC.

2019   Volume 9, Issue 1, p15423

Abstract

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 14C-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.
In text/plain format

Archived Files and Locations

application/pdf   1.4 MB
file_uzar6dchjrcbpogbijhm3tppci
repositori.udl.cat (web)
web.archive.org (webarchive)
Read Archived PDF
Preserved and Accessible
Type  article-journal
Stage   published
Date   2019-10-28
Language   en ?
Container Metadata
Open Access Publication
In DOAJ
In Keepers Registry
ISSN-L:  2045-2322
Work Entity
access all versions, variants, and formats of this works (eg, pre-prints)
Catalog Record
Revision: 971ee030-9074-44de-9772-29ac7e06f741
API URL: JSON