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    A recessive mutation was identified that constitutively activated the ethylene response pathway in Arabidopsis and resuited in a rosette-lethal phenotype. Positional cloning of the gene corresponding to this mutation revealed that it was allelic to responsive to antagonist1 (ran1), a mutation that causes seedlings to respond in a positive manner to what is normally a competitive inhibitor of ethylene binding. In contrast to the previously identified ran 1-1 and ran1-2 alleles that are morphologically indistinguishable from wild-type plants, this ran 1-3 allele results in a rosette-lethal phenotype. The predicted protien encoded by the RAN1 gene is similar to the Wilson menkes disease protiens and yeast Ccc2 protien, which are integral membrane cation-transporting P-type ATPases involved in copper trafficking. Genetic epistasis analysis indicated that RAN1 acts upstream of mutations in the ethylene receptor gene family. However, the rosette-lethal phenotype of ran1-3 was not suppressed by ethylene-insensitive mutants, sugesting that this mutation also affects a non-ethylene-dependent pathway regulating cell expansion. The phenotype of ran1-3 mutants is similar to loss-of-function ethylene receptor mutants, suggest that RAN1 may be required to form functional ethylene receptors. Furthermore, these results suggest taht copper is required not only for ethylene binding but also for the signaling function of the ethylene receptors.

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    Woeste, Keith; Kieber, Joseph J. 2000. A strong loss-of-function mutation in RAN1 results in constitution activation of the ethylene response pathway as well as a rosette-lethal phenotype. The Plant Cell. Volume 12. 2000. pp. 443-455


    Mutation, RAN1, ethylene, lethal phenotype, cloning, genetic

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