Arabidopsis RTE1 is essential to ethylene receptor ETR1 amino-terminal signaling independent of CTR1.

The Arabidopsis (Arabidopsis thaliana) ethylene receptor Ethylene Response1 (ETR1) can mediate the receptor signal output via its carboxyl terminus interacting with the amino (N) terminus of Constitutive Triple Response1 (CTR1) or via its N terminus (etr1¹⁻³⁴⁹ or the dominant ethylene-insensitive etr1-1¹⁻³⁴⁹) by an unknown mechanism. Given that CTR1 is essential to ethylene receptor signaling and that overexpression of Reversion To Ethylene Sensitivity1 (RTE1) promotes ETR1 N-terminal signaling, we evaluated the roles of CTR1 and RTE1 in ETR1 N-terminal signaling. The mutant phenotype of ctr1-1 and ctr1-2 was suppressed in part by the transgenes etr1¹⁻³⁴⁹ and etr1-1¹⁻³⁴⁹, with etr1-1 conferring ethylene insensitivity. Coexpression of 35S:RTE1 and etr1¹⁻³⁴⁹ conferred ethylene insensitivity in ctr1-1, whereas suppression of the ctr1-1 phenotype by etr1¹⁻³⁴⁹ was prevented by rte1-2. Thus, RTE1 was essential to ETR1 N-terminal signaling independent of the CTR1 pathway. An excess amount of the CTR1 N terminus CTR1⁷⁻⁵⁶⁰ prevented ethylene receptor signaling, and the CTR1⁷⁻⁵⁶⁰ overexpressor CTR1-Nox showed a constitutive ethylene response phenotype. Expression of the ETR1 N terminus suppressed the CTR1-Nox phenotype. etr1¹⁻³⁴⁹ restored the ethylene insensitivity conferred by dominant receptor mutant alleles in the ctr1-1 background. Therefore, ETR1 N-terminal signaling was not mediated by full-length ethylene receptors; rather, full-length ethylene receptors acted cooperatively with the ETR1 N terminus to mediate the receptor signal independent of CTR1. ETR1 N-terminal signaling may involve RTE1, receptor cooperation, and negative regulation by the ETR1 carboxyl terminus.