Mechanisms of natural and transgenic auxinic herbicide resistance

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Auxinic herbicides (e.g. 2,4-D, dicamba) were the first selective organic herbicides developed and have been used in agriculture for over 60 years primarily for the selective control of broadleaf weeds in cereal crops. They have revolutionized modern agriculture. If their use was eliminated because of severe weed resistance the total economic loss to Canadian farmers is estimated to be over $350 M/year, consisting of approximately $250 M due to crop loss and $100 M for the additional cost of replacement herbicides. The cost to consumers would be ca. $30-33 M in the first year, increasing to $300 M by year six. These herbicides are classified as mimics of indole-3-acetic acid (IAA), the natural plant hormone also known as auxin. Auxin has been implicated in virtually all aspects of plant growth and development. The incidence of auxinic herbicide resistance has increased. One of the most resistant weeds is a wild mustard (S. arvensis L.) biotype found in a Manitoba field treated with auxinic herbicides for over 10 years. My group was the first to characterize this resistant (R) biotype physiologically, biochemically, and genetically, thus furthering our understanding of the mechanism(s) of action of auxinic herbicides, and hence the mechanisms of action of auxin. The major goals of this research proposal are twofold: (1) identification of the gene responsible for auxinic herbicide resistance in wild mustard (S. arvensis), and (2) develop antibody (Ab)-based auxinic herbicide resistance, and expression of an anti-IAA Ab for auxin immunomodulation, in tobacco and Arabidopsis plants.  Knowledge gained from this research may identify a new auxin receptor class, may provide strategies to combat auxinic-herbicide resistance, allow development of novel herbicide resistance mechanisms for crop plants and new selectable markers for use in the production of transgenic plants, and novel physiological reagents for use in research towards a more complete understanding of auxinic herbicides and auxins.  Furthermore, expression of Abs against small molecules in plants may allow development of this mechanism as a practical model for creating Ab-based environmental contaminant resistance in plants for bioremediation of contaminated sites.