A genetic framework has been devised for the action of genes within the ethylene-response pathway. This working model is based on the epistatic interactions among a variety of ethylene response mutations. Most of the mutations that have been described act in a linear pathway. Genes controling cell elongation in response to ethylene must, at some level, act to affect the architecture of the cytoskeleton. Genes that act late in the pathway, in mutant form, may lead to highly specific phenotypes such as the increased senitivity to taxol in the ein6 mutant. Analysis of these downstream components may provide critical insights into the nature of ethylene's effect on the cell elongation machinery.