Figure 2

A model for the function of RAN1 in the ethylene signaling pathway. RAN1 is presumed to be localized in the membrane of a post-Golgi compartment. Copper ions received from CCH, a putative copper chaperon, is transported by RAN1 into a post-Golgi compartment, delivering the metal to membrane-targeted ethylene receptor apoproteins that become able to coordinate ethylene after the incorporation of copper ions. In the absence of the hormone, the receptors are active and negatively regulate downstream signaling components, preventing hormone-response phenotypes. Ethylene is expected to inactivate the receptors upon binding, presumably by causing a reduction in histidine kinase/phosphatase activity. This, in turn, results in derepression of downstream signaling components (EIN2, EIN3) and activation of hormone-response phenotypes. The metal-deficient ethylene receptors are nonfunctional, resulting in a constitutively activated signaling pathway.