The incidence of auxinic herbicide resistance in plants has increased worldwide. Auxinic herbicides were the first selective organic herbicides developed and have been used in agriculture for over 50 yr, primarily for the selective control of broadleaf weeds in cereal crops. However, the mode of action of auxinic herbicides and the molecular basis of auxinic herbicide resistance remain unknown, although an auxin-binding protein (ABP) is proposed to be the primary target site. Using auxinic herbicide-resistant (R) and -susceptible (S) biotypes of wild mustard as a model system, we have extensively studied the mode of action of auxinic herbicides and the resistance mechanisms at the physiological, biochemical, and molecular genetic levels. There are no differences in uptake, transport, and metabolism of auxinic herbicides between the R and S biotypes. Based on these results, as well as the studies on the role of auxin-enhanced ethylene biosynthesis and calcium in mediating the auxinic herbicide resistance, we hypothesize that resistance of the R biotype to auxinic herbicides is due to an altered target site, possibly an auxin receptor. We have identified and characterized a small ABP gene family as well as their cDNAs from both R and S of wild mustard. Amino acid changes were found in the ABP of the R biotype. Functional and mutational analyses of these genes are underway to determine the role of ABP in mediating auxinic herbicide resistance. In this review, we focus on the mode of action of auxinic herbicides and the molecular basis of auxinic herbicide resistance in wild mustard.

Nomenclature: 2,4-D; dicamba; MCPA; MCPP; picloram; ACC, 1-aminocyclopropane-1-carboxylic acid; MACC, 1-malonylaminocyclopropane-1-carboxylic acid; wild mustard, Brassica kaber (DC.) L.C.Wheeler SINAR.