4.4 Article

Thiobencarb resistance mechanism is distinct from CYP81A-based cross-resistance in late watergrass (Echinochloa phyllopogon)

Journal

WEED SCIENCE
Volume 70, Issue 2, Pages 160-166

Publisher

CAMBRIDGE UNIV PRESS
DOI: 10.1017/wsc.2022.4

Keywords

Cytochrome P450; metabolism-based herbicide resistance; non-target site resistance; segregation

Funding

  1. Japan Society for the Promotion of Science (JSPS) [17KI5234, 19H02955]
  2. Program for the Development of Next-Generation Leading Scientists with Global Insight (L-INSIGHT) - Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan
  3. Grants-in-Aid for Scientific Research [19H02955] Funding Source: KAKEN

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The genetic and molecular basis of resistance evolution in weeds to multiple herbicides, including those with unknown resistance mechanisms, was investigated in this study. A population of late watergrass was found to exhibit resistance to 15 herbicides, some of which were previously unknown. The resistance mechanism was found to be a combination of multiple factors, including cytochrome P450s and other unidentified non-target site mechanisms.
The genetic and molecular basis of resistance evolution in weeds to multiple herbicides remains unclear despite being a great threat to agriculture. A population of late watergrass [Echinochloa phyllopogon (Stapf.) Koso-Pol.] was reported to exhibit resistance to >= 15 herbicides from six sites of action, including thiobencarb (TB). While previous studies disclosed that the resistance to a majority of herbicides such as acetolactate synthase (ALS) and acetyl-CoA carboxylase inhibitors is caused by the overexpression of herbicide-metabolizing cytochrome P450s (CYP81A12 and CYP81A21), the resistance mechanisms to some herbicides remain unknown. Here, we analyzed the resistance segregation in the progenies between resistant and sensitive populations and performed a transgenic plant sensitivity assay to resolve whether TB resistance is endowed by the same CYP81A12/21-based cross-resistance mechanism or other unknown multiple-resistance mechanisms. In the F-6 progenies, resistance to the ALS inhibitor bensulfuron-methyl cosegregated with the resistances to many other herbicides under the CYP81A12/21-based cross-resistance mechanism; however, TB resistance segregated independently. Furthermore, CYP81A12/21 failed to confer TB resistance in transgenic Arabidopsis thaliana L. Heynh, thus confirming that TB resistance in resistant E. phyllopogon is not endowed by the two P450s that are responsible for the metabolism-based cross-resistance. This study provides evidence that resistance in E. phyllopogon to herbicides with multiple sites of action is endowed by both P450-based and other uncharacterized non-target site based mechanisms. Our findings add another layer in the understanding of resistance evolution to multiple herbicides in E. phyllopogon. Identification of the key genes endowing TB resistance will be the future direction of this research.

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