The gaseous plant hormone ethylene is perceived by a family of ethylene receptors and mediates an array of ethylene responses. In the absence of ethylene, receptor signaling is conveyed via the C-terminal histidine kinase domain to the N-terminus of the CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) protein kinase, which represses ethylene signaling mediated by ETHYLENE INSENSITIVE2 (EIN2) followed by EIN3. In the presence of ethylene, the receptors are inactivated when ethylene binds to their N-terminal domain, and consequently CTR1 is inactive, allowing EIN2 and EIN3 to activate ethylene signaling. Recent findings have shown that the ethylene receptor N-terminal portion can conditionally mediate the receptor signal output in mutants lacking CTR1, thus providing evidence of an alternative pathway from the ethylene receptors not involving CTR1. Here we highlight the evidence for receptor signaling to an alternative pathway and suggest that receptor signaling is coordinated via the N- and C-termini, as we address the biological significance of the negative regulation of ethylene signaling by the 2 pathways
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