迄今已经超过20年乙烯信号转导的研究已经建立一个相当完整、线性的信号转导模型。其中，CTR1是一个关键的信号组分: CTR1的突变体展现组成性的乙烯反应。然而，我们近年来的研究，发现在CTR1发生突变时，植物仍然能够条件性地通过替代途径抑制乙烯信号传递。我们课题组已经从多个方面研究该替代途径的重要性以及参与的组分。我们获得的一个CTR1 null突变体，展现非常微弱的组成性乙烯反应表型；这与之前所有关于CTR1的研究均不吻合。我们提出：植物在缺失CTR1的条件下，实际上并不会造成组成性乙烯反应，而是通过一个未知的替代途径完成乙烯信号的负调控。对此，我们设计了一系列的实验，获得更多的CTR1 null突变体来支持我们的假设。同时通过对CTR1 null突变体进行增强子筛选，从而获得替代途径的信号组分。我们初步结果已经获得更多的CTR1 nulls，也获得增强子突变体，暗示我们的假设存在正确性

To date, studies on ethylene signaling exceeds 20 years and a linear signal transduction pathway has been well established. CTR1 is considered a critical signaling component and CTR1 loss-of-function mutations result in constitutive ethylene responses. Contrast to the current model, our recent studies revealed presence of an alternative pathway that efficiently represses ethylene signaling independent of CTR1, thus only can CTR1 null alleles confer a weak degree of constitutive ethylene responses. These data are not in accordance with previously reported results. We herein propose that the typical constitutive ethylene response does not occur when CTR1 is absent and ethylene signaling in CTR1 nulls is efficiently prevented via an alternative pathway. To obtain supporting evidence, we carried out a series of experiments. Various CTR1 null alleles that were obtained did not confer a typical constitutive ethylene response phenotype. An enhancer screen we carried out for a CTR1 null isolated several enhancers and the double mutants exhibited a typical constitutive ethylene response phenotype. The preliminary data supported our hypothesis and thus our proposal is expectedly feasible. We expect to demonstrate that the alternative pathway has a role in ethylene signaling regulation and isolate the involved components once this proposal can be supported.