Possible modulation of Arabidopsis ETR1 N-terminal signaling by CTR1 |
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Authors: | Fang Xie Liping Qiu Chi-Kuang Wen |
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Affiliation: | National Key Laboratory of Plant Molecular Genetics and National Center for Plant Gene Research (Shanghai); Institute of Plant Physiology and Ecology; Shanghai Institutes for Biological Sciences; Chinese Academy of Sciences; Shanghai, China |
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Abstract: | The mitogen-activated protein kinase kinase kinase (MAPKKK) Constitutive Triple-Response1 (CTR1) plays a key role in mediating ethylene receptor signaling via its N-terminal interaction with the ethylene receptor C-terminal histidine kinase (HK) domain. Loss-of-function mutations of CTR1 prevent ethylene receptor signaling, and corresponding ctr1 mutants show a constitutive ethylene response phenotype. We recently reported in Plant Physiology that expression of the truncated ethylene receptor Ethylene Response1 (ETR1) isoforms etr11-349 and dominant ethylene-insensitive etr1-11-349, lacking the C-terminal HK and receiver domains, both suppressed the ctr1 mutant phenotype. Therefore, the ETR1 N terminus is capable of receptor signaling independent of CTR1. The constitutive ethylene response phenotype is stronger for ctr1-1 than ctr1-1 lines expressing the etr11-349 transgene, so N-terminal signaling by the full-length but not truncated ETR1 is inhibited by ctr1-1. We address possible modulations of ETR1 N-terminal signaling with docking of CTR1 on the ETR1 HK domain. |
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Keywords: | ethylene ethylene receptor ETR1 CTR1 ETR1 N-terminal signaling |
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