Ethylene Biosynthesis Following Foliar Application of Picloram to Biotypes of Wild Mustard (Sinapis arvensis L.) Susceptible or Resistant to Auxinic Herbicides

Abstract

Following foliar application of picloram (100 g a.i. ha−1) to biotypes of wild mustard (Sinapis arvensis L.) resistant (R) or susceptible (S) to auxinic herbicides, ethylene and its precursors, ACC (1-aminocyclopropane-1-carboxylic acid) and MAAC (1-malonylaminocyclopropane-1-carboxylic acid), as well as ACC synthase were quantified. Severe epinasty occurred within 24 hr after picloram was applied to the S biotype with concomitant increases in ACC synthase, ACC, MACC, and ethylene. No epinasty occurred in the R biotype, nor was there an increase above basal levels of ACC synthase, ACC, MACC, and ethylene in this biotype. Both biotypes became epinastic when fumigated with 120 μl liter−1 of ethylene. Furthermore, when the tissues from both biotypes were supplied with exogenous ACC (1 mM) after pretreatment with aminooxyacetic acid (1 mM), an inhibitor of ACC synthase, both biotypes produced ethylene thereby indicating that ethylene-forming enzyme was not impaired in the resistant biotype. These results suggest that picloram-induced ethylene biosynthesis in the S biotype of wild mustard results from de novo synthesis of ACC synthase; however, this is not the case in the R biotype. Furthermore, sensitivity differences between the two biotypes are related to regulation of picloram-induced ethylene biosynthesis and resistance may be due to a different interaction of the herbicide with primary target site(s) such as the auxin-binding protein(s).