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

机译:守卫细胞SLAC1通道的跨膜区域通过拟南芥中的ABA独立途径感知CO2信号。

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摘要

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 (). Several amino acids existing in the N-terminal region of SLAC1 are involved in regulating its activity via phosphorylation in the 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 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 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.
机译:保卫细胞S型阴离子通道SLOW阴离子通道1(SLAC1)是控制气孔运动的关键组件,可响应CO2和脱落酸而被激活。 SLAC1 N末端区域中存在的几种氨基酸通过响应中的磷酸化来调节其活性。然而,关于CO 2信号感知的位点知之甚少。为了解剖气孔CO2响应所必需的位点,我们使用表达截短的SLAC1蛋白的转基因植物进行了slac1互补实验。测量截短的转基因株系对CO2的气体交换和气孔孔径,并发现气孔CO2响应所涉及的位点存在于跨膜区域,不需要SLAC1 N和C末端。转基因品系的保卫细胞中的CO2和S型阴离子通道活性的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提高了暴露在膜上的两个酪氨酸残基参与气孔CO2反应的可能性。

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