Ethylene is not involved in clopyralid action in yellow starthistle ( Centaurea solstitialis L.)

Abstract

Auxinic herbicides often increase ethylene production in susceptible but not resistant plants. Thus, a role for ethylene biosynthesis in the resistance to, and mode of action of, auxinic herbicides has been suggested. Experiments were conducted to determine the role of ethylene production induced by clopyralid (3,6-dichloro-2-pyridine carboxylic acid) in the mode of action of, and cross-resistance to, this herbicide in picloram (4-amino-3,5,6-trichloro-2-pyridinecarboxylic acid)-susceptible (S) and -resistant (R) yellow starthistle ( Centaurea solstitialis L.) plants. Foliar-applied clopyralid induced ethylene production, epinasty, and necrosis in S but had no effect on R. Wounding induced ethylene production in both S and R, so R possesses a functional ethylene biosynthesis pathway. Aminoethoxyvinylglycine (AVG), an ethylene synthesis inhibitor, inhibited ethylene production in S; however, clopyralid-induced epinasty, necrosis, and shoot weight reduction were not prevented. Therefore, herbicide damage was not attributable to induced ethylene. In addition, silver thiosulfate (STS), an ethylene action inhibitor, did not alter herbicide damage. Foliar-applied ethephon, an ethylene-releasing compound, increased ethylene released from S and R, but did not visibly affect plants. Exogenous-applied ethylene in a flow-through system for 48 h did not induce morphological symptoms in plants at 0 or 250 μL L −1 ; at 500 μL L −1 and greater ethylene induced slight leaf rolling and wilting in both accessions although there was no effect on plant weight 3 weeks after treatment. The low sensitivity to exogenously applied ethylene and the inability of AVG and STS to block any symptoms induced by clopyralid suggest that ethylene is a symptom, not a mediator, of auxinic herbicide action and resistance in yellow starthistle.