Abstract

Summary The quinolinecarboxylic acid quinclorac, which is structurally related to natural auxins, is a rice herbicide with selective activity against dicot and monocot weeds. As demonstrated for monocot and dicot species, stimulation of ethylene production by the herbicide was positively correlated with its phytotoxic effect. Treatment of susceptible barnyardgrass plants (Echinocloa crus-galli) at the second leaf stage with 20 µtg/plant (approx. 3 × 10−5 mol·L−1) quinclorac via the root appeared to specifically induce ethylene biosynthesis in the root tissue. However, the 1-aminocyclopropane-1-carboxylic acid (ACC) produced and its derivatives predominantly accumulated in the shoot tissue, where levels of ACC, N-malonylACC (MACC), ethylene formation, and HCN increased up to 3-, 60-, 5-, and 3-fold, respectively. Concomitantly, intact root tissue was 50-fold less susceptible to damage by quinclorac than intact shoot tissue. The observed HCN level in the latter tissue went up from 12 to 38 µmol·L−1 after treatment with quinclorac. Among the other phytohormones analyzed, only the immunoreactive 3-indoleacetic acid content increased in shoot tissue. Additional treatment with the ACC synthase inhibitor aminoethoxyvinylglycine decreased quinclorac-induced ethylene production and the phytotoxic effects on shoots of barnyardgrass. Quinclorac-treated rice plants (Oryza sativa) showed no notable changes in ethylene production and endogenous ACC, MACC, HCN and immunoreactive phytohormone contents and, shoots of rice plants were 200-fold less susceptible to damage by quinclorac than those of barnyardgrass. In comparison with quinclorac, 2,4-dichlorophenoxyacetic acid (2,4-D) caused considerably lower increases in ethylene production and endogenous levels of ACC, MACC and HCN in barnyardgrass shoots. This coincided with a 30-fold lower phytotoxic effect of 2,4-D on this plant part. Furthermore, exogenously applied KCN caused phytotoxic symptoms on barnyardgrass very similar to those exerted by quinclorac. We suggest a possible relationship between phytotoxic susceptibility and accumulation of endogenous toxic HCN formed as a co-product during quinclorac-stimulated ethylene biosynthesis.

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