National Key Laboratory of Plant Molecular Genetics and National Center for Plant Gene Research, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200032, China.
Plant Physiol. 2012 Jul;159(3):1263-76. doi: 10.1104/pp.112.193979. Epub 2012 May 7.
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.
拟南芥（Arabidopsis thaliana）乙烯受体乙烯响应 1（ETR1）可以通过其羧基末端与组成型三重响应 1（CTR1）的氨基（N）末端相互作用（etr1¹⁻³⁴⁹ 或显性乙烯不敏感的 etr1-1¹⁻³⁴⁹）或通过其 N 末端（etr1¹⁻³⁴⁹ 或显性乙烯不敏感的 etr1-1¹⁻³⁴⁹）来介导受体信号输出，但具体机制尚不清楚。鉴于 CTR1 是乙烯受体信号传导所必需的，并且 Reversion To Ethylene Sensitivity1（RTE1）的过表达促进了 ETR1 N 末端信号传导，我们评估了 CTR1 和 RTE1 在 ETR1 N 末端信号传导中的作用。ctr1-1 和 ctr1-2 的突变表型部分被转基因 etr1¹⁻³⁴⁹ 和 etr1-1¹⁻³⁴⁹抑制，其中 etr1-1 赋予乙烯不敏感性。35S:RTE1 和 etr1¹⁻³⁴⁹ 的共表达赋予 ctr1-1 乙烯不敏感性，而 rte1-2 阻止了 etr1¹⁻³⁴⁹ 对 ctr1-1 表型的抑制。因此，RTE1 是 ETR1 N 末端信号传导所必需的，而不依赖于 CTR1 途径。过量的 CTR1 N 末端 CTR1⁷⁻⁵⁶⁰ 阻止了乙烯受体信号传导，而过量表达的 CTR1-Nox 表现出组成型乙烯反应表型。ETR1 N 末端的表达抑制了 CTR1-Nox 表型。etr1¹⁻³⁴⁹ 在 ctr1-1 背景下恢复了显性受体突变等位基因赋予的乙烯不敏感性。因此，ETR1 N 末端信号传导不是由全长乙烯受体介导的；相反，全长乙烯受体与 ETR1 N 末端协同作用，独立于 CTR1 介导受体信号。ETR1 N 末端信号传导可能涉及 RTE1、受体协作和 ETR1 羧基末端的负调控。
