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The ARP2/3 Complex Mediates Guard Cell Actin Reorganization and Stomatal Movement in Arabidopsis

机译:ARP2 / 3复合物介导拟南芥中保卫细胞肌动蛋白的重组和气孔运动。

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摘要

Guard cell actin reorganization has been observed in stomatal responses to a wide array of stimuli. However, how the guard cell signaling machinery regulates actin dynamics is poorly understood. Here, we report the identification of an allele of the Arabidopsis thaliana ACTIN-RELATED PROTEIN C2/DISTORTED TRICHOMES2 (ARPC2) locus (encoding the ARPC2 subunit of the ARP2/3 complex) designated high sugar response3 (hsr3). The hsr3 mutant showed increased transpirational water loss that was mainly due to a lesion in stomatal regulation. Stomatal bioassay analyses revealed that guard cell sensitivity to external stimuli, such as abscisic acid (), CaCl2, and light/dark transition, was reduced or abolished in hsr3. Analysis of a nonallelic mutant of the ARP2/3 complex suggested no pleiotropic effect of ARPC2 beyond its function in the complex in regard to stomatal regulation. When treated with , guard cell actin filaments underwent fast disruption in wild-type plants, whereas those in hsr3 remained largely bundled. The insensitivity phenotype of hsr3 was rescued by cytochalasin D treatment, suggesting that the aberrant stomatal response was a consequence of bundled actin filaments. Our work indicates that regulation of actin reassembly through ARP2/3 complex activity is crucial for stomatal regulation.
机译:在气孔对多种刺激的反应中观察到了保卫细胞肌动蛋白的重组。然而,保卫细胞信号转导机制如何调节肌动蛋白动力学了解甚少。在这里,我们报告鉴定为高糖反应3(hsr3)的拟南芥ACTIN相关蛋白C2 /扭曲的TRICHOMES2(ARPC2)基因座(编码ARP2 / 3复合物的ARPC2亚基)的等位基因。 hsr3突变体显示蒸腾失水增加,这主要是由于气孔调节中的病变所致。气孔生物测定分析表明,hsr3中保卫细胞对外部刺激(如脱落酸,CaCl2和明暗过渡)的敏感性降低或消失。 ARP2 / 3复合物的一个非等位基因突变体的分析表明,在气孔调节方面,ARPC2在复合物功能之外没有多效性作用。当用进行处理时,保卫细胞肌动蛋白丝在野生型植物中经历了快速破坏,而hsr3中的丝仍保持很大的束缚状态。 hsr3的不敏感表型通过细胞松弛素D处理得以挽救,这表明气孔异常反应是肌动蛋白丝束缚的结果。我们的工作表明,通过ARP2 / 3复合物活性调节肌动蛋白重组对于气孔调节至关重要。

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