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Effects of Tobacco Ethylene Receptor Mutations on Receptor Kinase Activity, Plant Growth and Stress Responses

机译:烟草乙烯受体突变对受体激酶活性,植物生长和胁迫响应的影响

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摘要

Ethylene receptor is the first component of ethylene signaling that regulates plant growth, development and stress responses. Previously, we have demonstrated that tobacco subfamily 2 ethylene receptor NTHK1 had Ser/Thr kinase activity, and overexpression of NTHK1 caused large rosette, reduced ethylene sensitivity, and increased salt sensitivity in transgenic Arabidopsis plants. Here we found that N-box mutation in the NTHK1 kinase domain abolished the kinase activity and led to disruption of NTHK1 roles in conferring reduced ethylene sensitivity and salt sensitive response in transgenic Arabidopsis plants. However, N-box mutation had partial effects on NTHK1 regulation of rosette growth and expression of salt- and ethylene-responsive genes AtNAC2, AtERF1 and AtCor6.6. Mutation of conserved residues in the H box did not affect kinase activity, seedling growth, ethylene sensitivity or salt-induced epinasty in transgenic plants but did influence NTHK1 function in control of specific salt- and ethylene-responsive gene expression. Compared with NTHK1, the tobacco subfamily 1 ethylene receptor NtETR1 had His kinase activity and played a weak role in regulation of rosette growth, triple response and salt response. Mutation of the conserved His residue in the NtETR1 H box eliminated phosphorylation and altered the effect of Ntetr1-1 on reporter gene activity. These results imply that the Ser/Thr kinase activity of NTHK1 is differentially required for various responses, and NTHK1 plays a larger role than NtETR1.
机译:乙烯受体是乙烯信号传导中调节植物生长,发育和胁迫响应的第一部分。以前,我们已经证明烟草亚家族2乙烯受体NTHK1具有Ser / Thr激酶活性,NTHK1的过表达引起大玫瑰花结,乙烯敏感性降低和盐敏感性提高。在这里,我们发现NTHK1激酶域中的N-box突变消除了激酶活性,并导致NTHK1在赋予转基因拟南芥植物降低的乙烯敏感性和盐敏感性响应的作用中受到破坏。但是,N-box突变对NTHK1的玫瑰花环生长以及盐和乙烯响应基因AtNAC2,AtERF1和AtCor6.6的表达有部分影响。 H盒中保守残基的突变不会影响转基因植物中的激酶活性,幼苗生长,乙烯敏感性或盐诱导的显性,但确实会影响NTHK1在控制特定盐和乙烯响应基因表达中的功能。与NTHK1相比,烟草亚家族1乙烯受体NtETR1具有His激酶活性,在调节玫瑰花结,三重反应和盐反应中起弱作用。 NtETR1 H盒中保守的His残基的突变消除了磷酸化,并改变了Ntetr1-1对报告基因活性的影响。这些结果表明NTHK1的Ser / Thr激酶活性是各种响应所必需的,并且NTHK1比NtETR1发挥更大的作用。

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