Ethylene responses are modulated by a family ot rive ethylene receptor members in Arabidopsis.The five receptors are genetically redundant while not functionally exchangeable; how the five receptor members may act coordinately remains elusive.We addressed this question by examining the signal output of transmitter-on ETR1 or ERS 1 in the absence of other wild-type receptors or in the presence of a wild-type receptor member.Converted to a singling active state by silver or 1-MCP, ETR1 alone was able to reverse ethylene growth inhibition to a great extent while ERS 1 was not.etr 1-1, ersl-1, and erslC65Y are transmitter-on receptor isoforms.etrl-1 substantially repressed ethylene responses in quintuple receptor knockout mutants while ersl-1 did not.The inhibition of ethylene responses by ersl-1 is mainly dependent on ETR1 or EIN4.EIN4 had a greater role than ETR1 in erslC65Y signaling.The lack of both ETR1 and EIN4 abolished the ability of erslC65Y in the repression of ethylene responses.We show that the wild-type receptors are not dispensable to the signal output of a transmitter-on ethylene receptor, implying collaborative receptor signaling.Receptor collaborations may facilitate a plant to make corresponding responses to a wide range of ethylene concentrations.Genetic redundancy and functional divergence of the five receptor members are essential to the maintenance of collaborative receptor signaling.