Extracellular malate induces stomatal closure via direct activation of guard‐cell anion channel SLAC1and stimulation of Ca2+ signalling
Extracellular malate induces stomatal closure via direct activation of guard‐cell anion channel SLAC1and stimulation of Ca2+ signalling
复制标题
细胞外苹果酸通过直接激活保卫细胞阴离子通道 SLAC1 和刺激 Ca2+ 信号传导诱导气孔关闭
DOI：
10.1111/nph.18400
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发表时间：
2022
期刊：
影响因子：
9.4
通讯作者：
Murata Yoshiyuki
中科院分区：
文献类型：
--
作者：
Mimata Yoshiharu;Munemasa Shintaro;Nakamura Toshiyuki;Nakamura Yoshimasa;Murata Yoshiyuki
植物在逆境条件下由保卫细胞向质外体分泌苹果酸，外源苹果酸诱导气孔关闭。苹果酸被认为是气孔关闭的细胞外化学信号。然而，苹果酸诱导气孔关闭的分子机制尚未完全阐明。我们研究了气孔开度、离子通道和胞质Ca 2+对苹果酸的响应。苹果酸诱导拟南芥野生型植物气孔关闭，但在慢（S型）阴离子通道基因SLOW ANION CHANNEL-ASSOCIATED 1（SLAC 1）缺陷的突变体中没有苹果酸处理增加了野生型植物保卫细胞原生质体中的S-型阴离子电流，但在lac 1突变体中没有。此外，在使用异种卵母细胞的异源表达系统中，细胞外而不是细胞内应用苹果酸增加了具有激酶非依赖性活性的SLAC 1组成型活性突变体的S型电流。结果表明，外源苹果酸可直接激活SLAC 1，并同时刺激保卫细胞内的Ca 2+信号，导致气孔关闭过程中SLAC 1的稳定激活。
Plants secrete malate from guard cells to apoplast under stress conditions and exogenous malate induces stomatal closure. Malate is considered an extracellular chemical signal of stomatal closure. However, the molecular mechanism of malate‐induced stomatal closure is not fully elucidated.We investigated responses of stomatal aperture, ion channels, and cytosolic Ca2+to malate.A treatment with malate induced stomatal closure inArabidopsis thalianawild‐type plants, but not in the mutants deficient in the slow (S‐type) anion channel geneSLOW ANION CHANNEL‐ASSOCIATED 1(SLAC1).The treatment with malate increased S‐type anion currents in guard‐cell protoplasts of wild‐type plants but not in theslac1mutant. In addition, extracellular rather than intracellular application of malate increased the S‐type currents of constitutively active mutants of SLAC1, which have kinase‐independent activities, in a heterologous expression system usingXenopusoocytes. The treatment with malate transiently increased cytosolic Ca2+concentration in the wild‐type Arabidopsis guard cells and the malate‐induced stomatal closure was inhibited by the Ca2+channel blocker and the Ca2+chelator.These results indicate that extracellular malate directly activates SLAC1 and simultaneously stimulates Ca2+signalling in guard cells, resulting in steady and solid activation of SLAC1 for stomatal closure.