Stomatal Closure by Fast Abscisic Acid Signaling Is Mediated by the Guard Cell Anion Channel SLAH3 and the Receptor RCAR1
Stomatal Closure by Fast Abscisic Acid Signaling Is Mediated by the Guard Cell Anion Channel SLAH3 and the Receptor RCAR1
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DOI：
10.1126/scisignal.2001346
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发表时间：
2011-05-17
影响因子：
7.3
通讯作者：
Hedrich, Rainer
中科院分区：
文献类型：
--
作者：
Geiger, Dietmar;Maierhofer, Tobias;Hedrich, Rainer
S 型阴离子通道是脱落酸 (ABA) 信号传导的直接目标，有助于保卫细胞释放氯离子和硝酸盐，进而启动气孔关闭。 SLAC1 是保卫细胞 S 型阴离子通道的第一个成分。然而，我们发现拟南芥SLAC1突变体的保卫细胞表现出硝酸盐电导。 SLAH3（SLAC1 同源物 3）也存在于保卫细胞中，SLAH3 与爪蟾卵母细胞中钙离子 (Ca2+) 依赖性激酶 CPK21 的共表达介导硝酸盐诱导的阴离子电流。硝酸盐、钙和磷酸化调节 SLAH3 活性。 CPK21 依赖性 SLAH3 磷酸化和激活被 ABI1 阻断，ABI1 是一种 PP2C 型蛋白磷酸酶，受 ABA 抑制，并抑制保卫细胞中的 ABA 信号通路。我们通过在反应中加入 ABA 受体-磷酸酶复合物 RCAR1-ABI1，在体外重建了 CPK21 对 ABA 刺激的 SLAH3 氨基末端结构域的磷酸化。我们提出，RCAR/PYR/PYL家族的ABA受体和ABI1组成的复合物对ABA的感知将CPK21从ABI1的抑制中释放出来，然后CPK21通过胞质Ca2+浓度的增加进一步激活，导致其SLAH3磷酸化。因此，将 SLAH3 鉴定为硝酸盐、钙和 ABA 敏感的保卫细胞阴离子通道，为了解气孔对干旱的反应、硝酸盐信号传导和硝酸盐代谢之间的关系提供了见解。
S-type anion channels are direct targets of abscisic acid (ABA) signaling and contribute to chloride and nitrate release from guard cells, which in turn initiates stomatal closure. SLAC1 was the first component of the guard cell S-type anion channel identified. However, we found that guard cells of Arabidopsis SLAC1 mutants exhibited nitrate conductance. SLAH3 (SLAC1 homolog 3) was also present in guard cells, and coexpression of SLAH3 with the calcium ion (Ca2+)-dependent kinase CPK21 in Xenopus oocytes mediated nitrate-induced anion currents. Nitrate, calcium, and phosphorylation regulated SLAH3 activity. CPK21-dependent SLAH3 phosphorylation and activation were blocked by ABI1, a PP2C-type protein phosphatase that is inhibited by ABA and inhibits the ABA signaling pathway in guard cells. We reconstituted the ABA-stimulated phosphorylation of the SLAH3 amino-terminal domain by CPK21 in vitro by including the ABA receptor-phosphatase complex RCAR1-ABI1 in the reactions. We propose that ABA perception by the complex consisting of ABA receptors of the RCAR/PYR/PYL family and ABI1 releases CPK21 from inhibition by ABI1, and then CPK21 is further activated by an increase in the cytosolic Ca2+ concentration, leading to its phosphorylation of SLAH3. Thus, the identification of SLAH3 as the nitrate-, calcium-, and ABA-sensitive guard cell anion channel provides insights into the relationship among stomatal response to drought, signaling by nitrate, and nitrate metabolism.