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The actin-related protein2/3 complex regulates mitochondrial-associated calcium signaling during salt stress in Arabidopsis.

机译:肌动蛋白相关蛋白2/3复合物在拟南芥盐胁迫期间调节线粒体相关的钙信号传导。

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摘要

Microfilament and Ca2+ dynamics play important roles in stress signaling in plants. Through genetic screening of Arabidopsis thaliana mutants that are defective in stress-induced increases in cytosolic Ca2+ ([Ca2+]cyt), we identified Actin-Related Protein2 (Arp2) as a regulator of [Ca2+]cyt in response to salt stress. Plants lacking Arp2 or other proteins in the Arp2/3 complex exhibited enhanced salt-induced increases in [Ca2+]cyt, decreased mitochondria movement, and hypersensitivity to salt. In addition, mitochondria aggregated, the mitochondrial permeability transition pore opened, and mitochondrial membrane potential Psi m was impaired in the arp2 mutant, and these changes were associated with salt-induced cell death. When opening of the enhanced mitochondrial permeability transition pore was blocked or increases in [Ca2+]cyt were prevented, the salt-sensitive phenotype of the arp2 mutant was partially rescued. These results indicate that the Arp2/3 complex regulates mitochondrial-dependent Ca2+ signaling in response to salt stress.
机译:微丝和Ca 2 + 动力学在植物胁迫信号中起重要作用。通过遗传筛选拟南芥突变体,这些突变体在胁迫诱导的胞质Ca 2 + ([Ca 2 + ] cyt )的增加中存在缺陷,我们确定肌动蛋白相关蛋白2(Arp2)是盐胁迫下[Ca 2 + ] cyt 的调节因子。在Arp2 / 3复合物中缺少Arp2或其他蛋白质的植物表现出增强的盐诱导[Ca 2 + ] cyt 增加,线粒体运动减少和对盐超敏性。此外,arp2突变体中线粒体聚集,线粒体通透性过渡孔打开,线粒体膜电位Psi m受损,这些变化与盐诱导的细胞死亡有关。当增强的线粒体通透性过渡孔的开放被阻止或[Ca 2 + ] cyt 的增加被阻止时,arp2突变体的盐敏感性表型得以部分挽救。这些结果表明Arp2 / 3复合物响应盐胁迫而调节线粒体依赖性Ca 2 + 信号传导。

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