Effects of Mecoprop (an Auxin Analogue) on Ethylene Evolution and Epinasty in Two Biotypes of Stellaria media

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Abstract
Petiolar epinasty and the production of ethylene (ethene) were studied in chickweed biotypes, Stellaria media, treated with the herbicide and auxin analogue (RS)-2-(4-chloro-o-tolyloxy)propionic acid, potassium salt, common name mecoprop. This compound caused severe epinasty and stimulated the production of ethylene from shoot explants. However, when intact plants were treated with ethylene, the leaves became only slightly epinastic. The ethylene precursor, 1-aminocyclopropane-I-carboxylic acid (ACC), at concentrations which stimulated the release of ethylene, was equally ineffective in causing epinasty. Furthermore, 2, 5-norbornadiene, a specific, competitive inhibitor of ethylene action, only partly alleviated mecoprop-induced epinasty. The responses observed in chickweed were compared with those produced in tomato plants. ACC induced epinasty in tomato within 2 h and these symptoms were completely inhibited by norbornadiene. However, as in chickweed, the inhibitor gave only partial reversal of mecoprop-induced epinasty, implying that the epinastic response caused by the herbicide was not attributable to ethylene alone. We therefore suggest that mecoprop-induced epinasty is a result of the combined ethylene-stimulating and growth-promoting properties of the herbicide. Mecoprop-stimulated ethylene evolution was initially significantly greater in a herbicide-resistant, compared with a more susceptible biotype of chickweed. The significance of this finding is discussed in relation to the mechanism of mecoprop resistance in chickweed.

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