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A strong constitutive ethylene-response phenotype conferred on Arabidopsis plants containing null mutations in the ethylene receptors ETR1 and ERS1

Qu, Xiang and Hall, Brenda P. and Gao, Zhiyong and Schaller, G. Eric (2007) A strong constitutive ethylene-response phenotype conferred on Arabidopsis plants containing null mutations in the ethylene receptors ETR1 and ERS1. BMC Plant Biology, 7 . Art. No. 3. ISSN 1471-2229. PMCID PMC1781942.

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Background: The ethylene receptor family of Arabidopsis consists of five members, falling into two subfamilies. Subfamily 1 is composed of ETR1 and ERS1, and subfamily 2 is composed of ETR2, ERS2, and EIN4. Although mutations have been isolated in the genes encoding all five family members, the only previous insertion allele of ERS1 (ers1-2) is a partial loss-of-function mutation based on our analysis. The purpose of this study was to determine the extent of signaling mediated by subfamily-1 ethylene receptors through isolation and characterization of null mutations. Results: We isolated new T-DNA insertion alleles of subfamily 1 members ERS1 and ETR1 (ers1-3 and etr1-9, respectively), both of which are null mutations based on molecular, biochemical, and genetic analyses. Single mutants show an ethylene response similar to wild type, although both mutants are slightly hypersensitive to ethylene. Double mutants of ers1-3 with etr1-9, as well as with the previously isolated etr1-7, display a constitutive ethylene-response phenotype more pronounced than that observed with any previously characterized combination of ethylene receptor mutations. Dark-grown etr1-9;ers1-3 and etr1-7;ers1-3 seedlings display a constitutive triple-response phenotype. Light-grown etr1-9;ers1-3 and etr1-7;ers1-3 plants are dwarfed, largely sterile, exhibit premature leaf senescence, and develop novel filamentous structures at the base of the flower. A reduced level of ethylene response was still uncovered in the double mutants, indicating that subfamily 2 receptors can independently contribute to signaling, with evidence suggesting that this is due to their interaction with the Raf-like kinase CTR1. Conclusion: Our results are consistent with the ethylene receptors acting as redundant negative regulators of ethylene signaling, but with subfamily 1 receptors playing the predominant role. Loss of a single member of subfamily 1 is largely compensated for by the activity of the other member, but loss of both subfamily members results in a strong constitutive ethylene-response phenotype. The role of subfamily 1 members is greater than previously suspected and analysis of the double mutant null for both ETR1 and ERS1 uncovers novel roles for the receptors not previously characterized.

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Additional Information:© 2007 Qu et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Received 6 July 2006. Accepted 15 January 2007. Published 15 January 2007. This work was supported by grants from the National Science Foundation (MCB-0235450 and MCB-0430191) and from the Department of Energy (DE-FG02-05ER15704) to GES. We thank Dr. Dennis E. Mathews (Univ. New Hampshire) for assistance with the initial T-DNA screens. Authors' contributions: XQ isolated and characterized mutations, transformed etr1-9;ers1-3 with the ETR1 construct, and helped to draft the manuscript. BPH identified homozygous etr1-9;ers1-3 lines containing the ETR1 construct, performed molecular and physiological characterizations of mutants and transformed lines, and helped to draft the manuscript. ZG analyzed CTR1 levels in the mutants. GES conceived and coordinated the study, performed physiological characterizations, and drafted the manuscript. All authors read and approved the final manuscript.
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Department of Energy (DOE)DE-FG02-05ER15704
PubMed Central ID:PMC1781942
Record Number:CaltechAUTHORS:QUXbmcpb07
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Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:7319
Deposited By: Archive Administrator
Deposited On:30 Jan 2007
Last Modified:02 Oct 2019 23:40

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