Auxinic Herbicide Resistance May Be Modulated at the Auxin-Binding Site in Wild Mustard (Sinapis arvensis L.): A Light Scattering Study

The effects of IAA and the auxinic herbicides picloram and MCPP on the flash-induced nucleotide-independent light-scattering signal from picloram-resistant (R) and- susceptible (S) wild mustard (Sinapis arvensis L.) protoplasts were studied. We previously demonstrated that an increase in H+ efflux leads to a decrease in amplitude of the light-scattering signal. In this study, IAA increased H+ efflux (i.e., decreased the signal amplitude) in both R and S protoplasts in direct proportion to the IAA concentration. When the signal amplitudes from picloram-treated R and S biotype were compared, they were different. Picloram, which adversely affects the S biotype in vivo and in vitro, increased H+ efflux (reduced signal amplitude) in S protoplasts but did not affect H+ efflux in R. MCPP, which adversely affects both biotypes in vivo and in vitro, increased H+ efflux in both biotypes. Preincubation of S protoplasts with IAA did not alter the effects of picloram or MCPP on H+ efflux (i.e., increased efflux). Conversely, preincubation of R protoplasts with IAA reduced MCPPmediated H+ efflux thereby reducing the adverse affects of MCPP. These results support our hypothesis that the physiological basis for this auxinic herbicide resistance in the wild mustard biotype is associated with their altered binding to auxin binding sites.