Interplay of Plasma Membrane and Vacuolar Ion Channels, Together with BAK1, Elicits Rapid Cytosolic Calcium Elevations in Arabidopsis during Aphid Feeding
Interplay of Plasma Membrane and Vacuolar Ion Channels, Together with BAK1, Elicits Rapid Cytosolic Calcium Elevations in Arabidopsis during Aphid Feeding
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DOI：
10.1105/tpc.17.00136
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发表时间：
2017-06-01
期刊：
影响因子：
11.6
通讯作者：
Sanders, Dale
中科院分区：
文献类型：
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作者：
Vincent, Thomas R.;Avramova, Marieta;Sanders, Dale
细胞质钙离子浓度的瞬时升高是植物感知环境的主要信号之一。钙在检测非生物胁迫中的作用是有据可查的，然而，它在生物相互作用中的作用仍然不清楚。在这里，我们使用的荧光钙生物传感器（GCaMP 3）结合绿色桃蚜（桃蚜）作为一种工具，研究拟南芥钙动态在体内和真实的时间在一个活的生物相互作用。我们证明了快速和高度本地化的植物钙升高周围的喂养网站的M。通过对蚜虫取食行为的电生理监测，我们证明了这些海拔与蚜虫对表皮和叶肉细胞的探测有关。此外，我们剖析了所涉及的分子机制，表明植物防御辅助受体油菜甾醇不敏感相关激酶1（BAK1），质膜离子通道谷氨酸受体样3.3和3.6（GLR 3.3和GLR 3.6），和液泡离子通道双孔通道1（TPC 1）之间的相互作用介导这些钙离子升高。因此，我们确定了植物感知生物威胁BAK1，细胞钙离子进入介导的GLR，和细胞内钙释放TPC 1在生物相关的相互作用之间的联系。
A transient rise in cytosolic calcium ion concentration is one of the main signals used by plants in perception of their environment. The role of calcium in the detection of abiotic stress is well documented; however, its role during biotic interactions remains unclear. Here, we use a fluorescent calcium biosensor (GCaMP3) in combination with the green peach aphid (Myzus persicae) as a tool to study Arabidopsis thaliana calcium dynamics in vivo and in real time during a live biotic interaction. We demonstrate rapid and highly localized plant calcium elevations around the feeding sites of M. persicae, and by monitoring aphid feeding behavior electrophysiologically, we demonstrate that these elevations correlate with aphid probing of epidermal and mesophyll cells. Furthermore, we dissect the molecular mechanisms involved, showing that interplay between the plant defense coreceptor BRASSINOSTEROID INSENSITIVE-ASSOCIATED KINASE1 (BAK1), the plasma membrane ion channels GLUTAMATE RECEPTOR-LIKE 3.3 and 3.6 (GLR3.3 and GLR3.6), and the vacuolar ion channel TWO-PORE CHANNEL1 (TPC1) mediate these calcium elevations. Consequently, we identify a link between plant perception of biotic threats by BAK1, cellular calcium entry mediated by GLRs, and intracellular calcium release by TPC1 during a biologically relevant interaction.