Canonical histidine kinase activity of the transmitter domain of the ETR1 ethylene receptor from Arabidopsis is not required for signal transmission

被引:176
作者
Wang, WY
Hall, AE
O'Malley, R
Bleecker, AB [1 ]
机构
[1] Univ Wisconsin, Dept Bot, Madison, WI 53706 USA
[2] Univ Wisconsin, Genet Lab, Madison, WI 53706 USA
关键词
D O I
10.1073/pnas.0237085100
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Ethylene signaling in plants is mediated by a family of receptors related to bacterial two-component histidine kinases. Of the five members of the Arabidopsis ethylene receptor family, members of subfamily I (ETR1 and ERS1) contain completely conserved histidine kinase domains, whereas members of subfamily II (ETR2, EIN4, and ERS2) lack conserved residues thought to be necessary for kinase activity. To examine the role of the conserved histidine kinase domain in receptor signaling, ers1;etr1 loss-of-function double mutants were generated. The double mutants exhibited a severe constitutive ethylene response phenotype consistent with the negative regulator model for receptor function. The adult err1-2,etr1-6 and ers1-2,etr1-7 phenotypes included miniature rosette size, delayed flowering, and both male and female sterility, whereas etiolated-seedling responses were less affected. Chimeric transgene constructs in which the ETR1 promoter was used to drive expression of cDNAs for each of the five receptor isoforms were transferred into the ers1-2,etr1-7double-mutant plants. Subfamily I constructs restored normal growth, whereas subfamily II constructs failed to rescue the double mutant, providing evidence for a unique role for subfamily I in receptor signaling. However, transformation of either the ers1-2,etr1-6 or ers1-2,etr1-7 mutant with a kinase-in activated ETR1 genomic clone also resulted in complete restoration of normal growth and ethylene responsiveness in the double-mutant background, leading to the conclusion that canonical histidine kinase activity by receptors is not required for ethylene receptor signaling.
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页码:352 / 357
页数:6
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