Evolved polygenic herbicide resistance in Lolium rigidum by low-dose herbicide selection within standing genetic variation

Authors

  • Roberto Busi,

    Corresponding author
    • Australian Herbicide Resistance Initiative, School of Plant Biology, UWA Institute of Agriculture, University of Western Australia, Crawley, WA, Australia
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  • Paul Neve,

    1. School of Life Sciences, Warwick University, Warwick HRI, Wellesbourne, Warwick, UK
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  • Stephen Powles

    1. Australian Herbicide Resistance Initiative, School of Plant Biology, UWA Institute of Agriculture, University of Western Australia, Crawley, WA, Australia
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Correspondence

Roberto Busi, Australian Herbicide Resistance Initiative, School of Plant Biology, UWA Institute of Agriculture, University of Western Australia, Crawley, WA, Australia.

Tel.: +61 08 6488 1423;

fax: +61 08 6488 7834;

e-mail: roberto.busi@uwa.edu.au

Abstract

The interaction between environment and genetic traits under selection is the basis of evolution. In this study, we have investigated the genetic basis of herbicide resistance in a highly characterized initially herbicide-susceptible Lolium rigidum population recurrently selected with low (below recommended label) doses of the herbicide diclofop-methyl. We report the variability in herbicide resistance levels observed in F1 families and the segregation of resistance observed in F2 and back-cross (BC) families. The selected herbicide resistance phenotypic trait(s) appear to be under complex polygenic control. The estimation of the effective minimum number of genes (NE), depending on the herbicide dose used, reveals at least three resistance genes had been enriched. A joint scaling test indicates that an additive-dominance model best explains gene interactions in parental, F1, F2 and BC families. The Mendelian study of six F2 and two BC segregating families confirmed involvement of more than one resistance gene. Cross-pollinated L. rigidum under selection at low herbicide dose can rapidly evolve polygenic broad-spectrum herbicide resistance by quantitative accumulation of additive genes of small effect. This can be minimized by using herbicides at the recommended dose which causes high mortality acting outside the normal range of phenotypic variation for herbicide susceptibility.

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