Abstract
BackgroundThe signal output of ethylene receptor family members is mediated by unknown mechanisms to activate the Raf-like protein CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) in negatively regulating ethylene signaling. The physical interaction between the ethylene receptor histidine kinase (HK) domain and CTR1 N terminus is essential to the CTR1-mediated receptor signal output. To advance our knowledge of the involvement of CTR1-mediated ethylene receptor signaling, we performed a genetic screen for mutations that enhanced the constitutive ethylene response in the weak ctr1-10 allele.ResultsWe isolated a loss-of-function allele of ENHANCING ctr1-10 ETHYLENE RESPONSE2 (ECR2) and found that ecr2-1 ctr1-10 and the strong allele ctr1-1 conferred a similar, typical constitutive ethylene response phenotype. Genetic analyses and transformation studies suggested that ECR2 acts downstream of the ethylene receptors and upstream of the transcription factors ETHYLENE INSENSITIVE3 (EIN3) and EIN3-LIKE1 (EIL1), which direct the expression of ethylene response genes. Signal output by the N terminus of the ethylene receptor ETHYLENE RESPONSE1 (ETR1) can be mediated by a pathway independent of CTR1. Expression of the N terminus of the ethylene-insensitive etr1-1 but not the full-length isoform rescued the ecr2-1 ctr1-10 phenotype, which indicates the involvement of ECR2 in CTR1-mediated but not -independent, ethylene receptor signaling. ECR2 was mapped to the centromere region on chromosome 2. With incomplete sequence and annotation information and rare chromosome recombination events in this region, the cloning of ECR2 is challenging and still in progress.ConclusionsECR2 is a novel allele involved in the ethylene receptor signaling that is mediated by CTR1. CTR1 activation by ethylene receptors may require ECR2 for suppressing the ethylene response.
Highlights
The signal output of ethylene receptor family members is mediated by unknown mechanisms to activate the Raf-like protein CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) in negatively regulating ethylene signaling
We considered 3 scenarios explaining the synergistic effect of ecr2-1 and ctr1-10: 1) ECR2 could be required in part for CTR1 activity or the protein stability, 2) ECR2 and CTR1 act in different pathways, or 3) ECR2 could be a signaling molecule acting with CTR1 to suppress the ethylene signaling
Little is known about the presence of any other components that are involved in the ethylene receptor signaling to CTR1
Summary
The signal output of ethylene receptor family members is mediated by unknown mechanisms to activate the Raf-like protein CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) in negatively regulating ethylene signaling. The physical interaction between the ethylene receptor histidine kinase (HK) domain and CTR1 N terminus is essential to the CTR1-mediated receptor signal output. The dicotyledonous model plant Arabidopsis has five ethylene receptors that physically act at the endoplasmic reticulum (ER) with the Raf-like protein CONSTITUTIVE TRIPLE-RESPONSE1 (CTR1) to negatively regulate ethylene signaling [1,2,3,4]. CTR1 has serine/threonine kinase activity, and the ethylene response is inversely associated with CTR1 kinase activity [4,15] These studies suggest that the HK domain mediates ethylene receptor signaling to the CTR1 N terminus, activating CTR1 to suppress the ethylene response, the underlying biochemical mechanisms are elusive
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