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拟南芥保卫细胞SLAC1通道的跨膜区域通过一条不依赖脱落酸的途径感知二氧化碳信号。

The Transmembrane Region of Guard Cell SLAC1 Channels Perceives CO2 Signals via an ABA-Independent Pathway in Arabidopsis.

作者信息

Yamamoto Yoshiko, Negi Juntaro, Wang Cun, Isogai Yasuhiro, Schroeder Julian I, Iba Koh

机构信息

Department of Biology, Faculty of Science, Kyushu University, Motooka, Nishi-ku, Fukuoka 819-0395, Japan.

Cell and Developmental Biology Section, Division of Biological Sciences, University of California at San Diego, La Jolla, California 92093.

出版信息

Plant Cell. 2016 Feb;28(2):557-67. doi: 10.1105/tpc.15.00583. Epub 2016 Jan 13.

Abstract

The guard cell S-type anion channel, SLOW ANION CHANNEL1 (SLAC1), a key component in the control of stomatal movements, is activated in response to CO2 and abscisic acid (ABA). Several amino acids existing in the N-terminal region of SLAC1 are involved in regulating its activity via phosphorylation in the ABA response. However, little is known about sites involved in CO2 signal perception. To dissect sites that are necessary for the stomatal CO2 response, we performed slac1 complementation experiments using transgenic plants expressing truncated SLAC1 proteins. Measurements of gas exchange and stomatal apertures in the truncated transgenic lines in response to CO2 and ABA revealed that sites involved in the stomatal CO2 response exist in the transmembrane region and do not require the SLAC1 N and C termini. CO2 and ABA regulation of S-type anion channel activity in guard cells of the transgenic lines confirmed these results. In vivo site-directed mutagenesis experiments targeted to amino acids within the transmembrane region of SLAC1 raise the possibility that two tyrosine residues exposed on the membrane are involved in the stomatal CO2 response.

摘要

保卫细胞S型阴离子通道SLOW ANION CHANNEL1(SLAC1)是控制气孔运动的关键组成部分,它在响应二氧化碳和脱落酸(ABA)时被激活。SLAC1 N端区域存在的几个氨基酸通过ABA响应中的磷酸化作用参与调节其活性。然而,对于参与二氧化碳信号感知的位点了解甚少。为了剖析气孔对二氧化碳响应所必需的位点,我们使用表达截短型SLAC1蛋白的转基因植物进行了slac1互补实验。对截短型转基因系中响应二氧化碳和ABA的气体交换及气孔孔径的测量表明,参与气孔对二氧化碳响应的位点存在于跨膜区域,且不需要SLAC1的N端和C端。转基因系保卫细胞中S型阴离子通道活性的二氧化碳和ABA调节证实了这些结果。针对SLAC1跨膜区域内氨基酸的体内定点诱变实验增加了膜上暴露的两个酪氨酸残基参与气孔对二氧化碳响应的可能性。

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