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AtGSK1的组成型过表达在无NaCl胁迫的情况下诱导NaCl胁迫反应,并导致拟南芥对NaCl耐受性增强。

Constitutive over-expression of AtGSK1 induces NaCl stress responses in the absence of NaCl stress and results in enhanced NaCl tolerance in Arabidopsis.

作者信息

Piao H L, Lim J H, Kim S J, Cheong G W, Hwang I

机构信息

Center for Plant Intracellular Trafficking, Pohang University of Science and Technology, Pohang, 790-784, Korea.

出版信息

Plant J. 2001 Aug;27(4):305-14. doi: 10.1046/j.1365-313x.2001.01099.x.

Abstract

GSK3/shaggy-like protein kinases have been shown to play diverse roles in development and signal transduction pathways in various organisms. An Arabidopsis homologue of GSK3/shaggy-like kinase, AtGSK1, has been shown to be involved in NaCl stress responses. In order to further clarify the role of AtGSK1 in NaCl stress responses in plants, we generated transgenic Arabidopsis plants that over-expressed AtGSK1 mRNA. These plants showed enhanced resistance to NaCl stress when assayed either as whole plants or by measurement of root growth on NaCl plates. In addition, AtGSK1 transgenic plants in the absence of NaCl stress showed phenotypic changes, such as accumulation of anthocyanin, that were similar to those observed in wild-type plants under NaCl stress. Transgenic plants accumulated 30-50% more Na+ than did wild-type plants when subjected to NaCl stress, and Ca2+ content was increased by 15-30% in the transgenic plants regardless of the NaCl stress level. Northern blotting revealed that AtGSK1 over-expression induced expression of the NaCl stress-responsive genes AtCP1, RD29A and CHS1 in the absence of NaCl stress. In addition, AtCBL1 and AtCP1 were super-induced in the NaCl-stressed transgenic plants. Taken together, these results suggest that AtGSK1 is involved in the signal transduction pathway(s) of NaCl stress responses in Arabidopsis.

摘要

糖原合成酶激酶3/类Shaggy蛋白激酶已被证明在多种生物体的发育和信号转导途径中发挥着不同作用。拟南芥中糖原合成酶激酶3/类Shaggy激酶的同源物AtGSK1,已被证明参与NaCl胁迫反应。为了进一步阐明AtGSK1在植物NaCl胁迫反应中的作用,我们构建了过表达AtGSK1 mRNA的转基因拟南芥植株。当以整株植物进行测定或以在NaCl平板上测量根生长的方式进行检测时,这些植株对NaCl胁迫表现出增强的抗性。此外,在没有NaCl胁迫的情况下,AtGSK1转基因植株表现出表型变化,如积累花青素,这与野生型植物在NaCl胁迫下观察到的表型变化相似。当受到NaCl胁迫时,转基因植株积累的Na+比野生型植株多30 - 50%,并且无论NaCl胁迫水平如何,转基因植株中的Ca2+含量增加了15 - 30%。Northern印迹分析表明,在没有NaCl胁迫的情况下,AtGSK1的过表达诱导了NaCl胁迫响应基因AtCP1、RD29A和CHS1的表达。此外,AtCBL1和AtCP1在受到NaCl胁迫的转基因植株中被超诱导。综上所述,这些结果表明AtGSK1参与了拟南芥中NaCl胁迫反应的信号转导途径。

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