Inheritance of fomesafen and imazethapyr resistance in a multiple herbicide‐resistant Euphorbia heterophylla population

2020 
Euphorbia heterophylla populations endued with resistance to both imazethapyr (an acetolactate synthase inhibitor) and fomesafen (a protoporphyrinogen oxidase inhibitor) were first detected in Brazil in 2004. The objectives of this study were to determine the number and dominance of genes conferring imazethapyr and fomesafen resistance in E. heterophylla and to establish the types of inheritance of the resistance traits. It was hypothesised that two dominant nuclear genes control this herbicide resistance and each gene confers resistance to a single herbicide. We crossed a susceptible (S) and a multiple‐resistant (R) E. heterophylla biotype and generated F₁ families which, in turn, were self‐fertilised to produce F₂ families. Backcrosses of the F₁ families with the S‐ and R parental biotypes resulted in BCₛ and BCᵣ families respectively. The F₁, F₂, BCₛ and BCᵣ families and the S and R parental biotypes were subjected to imazethapyr and fomesafen wherein each herbicide was used as a selecting agent. F₁ plants and the S‐ and R parental biotypes were used to evaluate the dominance of the resistance trait in multiple‐dose bioassays with imazethapyr and fomesafen. The observed frequencies of resistant plants in the F₁, F₂, BCₛ and BCᵣ families did not significantly differ from the expected frequencies for a resistance trait regulated by two dominant genes in which each gene confers resistance to a single herbicide. The lack of difference in herbicide response between the F₁ family and the R parental biotype was taken as evidence for completely dominant resistance to imazethapyr and fomesafen. Herbicide resistance in E. heterophylla presents with dominant monogenic nuclear inheritance for each herbicide mode of action. Our findings underscore the necessity and urgency of adopting integrated strategies to control E. heterophylla and to inhibit the evolution of new herbicide‐resistant strains.
    • Correction
    • Source
    • Cite
    • Save
    • Machine Reading By IdeaReader
    28
    References
    0
    Citations
    NaN
    KQI
    []