Mutations in the SLAC1 anion channel slow stomatal opening and severely reduce K+ uptake channel activity via enhanced cytosolic [Ca2+] and increased Ca2+ sensitivity of K+ uptake channels.
Mutations in the SLAC1 anion channel slow stomatal opening and severely reduce K+ uptake channel activity via enhanced cytosolic [Ca2+] and increased Ca2+ sensitivity of K+ uptake channels.
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DOI：
10.1111/nph.12008
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发表时间：
2013-01
期刊：
影响因子：
--
通讯作者：
Kollist H
中科院分区：
文献类型：
--
作者：
Laanemets K;Wang YF;Lindgren O;Wu J;Nishimura N;Lee S;Caddell D;Merilo E;Brosche M;Kilk K;Soomets U;Kangasjärvi J;Schroeder JI;Kollist H
拟南芥保卫细胞阴离子通道SLAC1在气孔关闭过程中起重要作用。有趣的是，在这里，我们揭示了一个意想不到的slac1等位基因对气孔开放的损害。我们报告说，突变SLAC1出乎意料地缓慢气孔开放诱导的光，低CO2和空气湿度升高在完整的植物，这是由严重降低活性的内向K+（K+在）通道slac1保卫细胞。气孔开放的通道和转运蛋白的表达表现出小，但显着减少slac1保卫细胞的转录水平，但这被认为是不足以解释严重受损的钾离子通道活性slac1。我们进一步检查了静息胞浆[Ca2+]cyt水平和slac1中K+通道对胞浆[Ca2+]cyt的敏感性。这些实验表明，slac1保卫细胞中静息[Ca2+]cyt较高，将[Ca2+]cyt降低至<10 nM可迅速恢复slac1通道中K+的活性，使其接近野生型水平。这些研究结果表明，在植物气孔调节，抵消受损的气孔关闭响应slac1，通过下调气孔开放机制和牵连增强[Ca2+]细胞敏感性启动作为一个机制基础下调K+通道活性的补偿反馈控制。
The Arabidopsis guard cell anion channel SLAC1 is essential for stomatal closure in response to various endogenous and environmental stimuli. Interestingly, here we reveal an unexpected impairment of slac1 alleles on stomatal opening. We report that mutations in SLAC1 unexpectedly slow stomatal opening induced by light, low CO2 and elevated air humidity in intact plants and that this is caused by the severely reduced activity of inward K+ (K+in) channels in slac1 guard cells. Expression of channels and transporters involved in stomatal opening showed small, but significant reductions in transcript levels in slac1 guard cells, however this was deemed insufficient to explain the severely impaired K+in channel activity in slac1. We further examined resting cytosolic [Ca2+]cyt levels and K+in channel sensitivity to cytosolic [Ca2+]cyt in slac1. These experiments showed higher resting [Ca2+]cyt in slac1 guard cells and that reducing [Ca2+]cyt to <10 nM rapidly restored the activity of K+in channels in slac1 closer to wild type levels. These findings demonstrate an unanticipated compensatory feedback control in plant stomatal regulation, that counteracts the impaired stomatal closing response of slac1, by down-regulating stomatal opening mechanisms and implicates enhanced [Ca2+]cyt sensitivity priming as a mechanistic basis for the down-regulated K+in channel activity.
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影响因子：
11.4
作者：
HEDRICH, R;BUSCH, H;RASCHKE, K
通讯作者：
RASCHKE, K
DOI：
10.1073/pnas.0912021106
发表时间：
2009-12-15
影响因子：
11.1
作者：
Geiger, Dietmar;Scherzer, Soenke;Hedrich, Rainer
通讯作者：
Hedrich, Rainer
DOI：
10.1073/pnas.0709732105
发表时间：
2008-04-01
影响因子：
11.1
作者：
Lebaudy, Anne;Vavasseur, Alain;Sentenac, Herve
通讯作者：
Sentenac, Herve
影响因子：
7.4
作者：
Grabov, A;Blatt, MR
通讯作者：
Blatt, MR
DOI：
10.1073/pnas.1116590109
发表时间：
2012-06-26
影响因子：
11.1
作者：
Brandt, Benjamin;Brodsky, Dennis E.;Schroeder, Julian I.
通讯作者：
Schroeder, Julian I.