Li Jiajing, Lu Pengfei, Pan Qing, Wang Bingxiao, Wang Youjun, Li Jiejie
Beijing Key Laboratory of Gene Resource and Molecular Development, College of Life Science, Beijing Normal University, Beijing 100875, China; Guangdong Institute of Intelligence Science and Technology, Hengqin, Zhuhai 519031, China.
Beijing Key Laboratory of Gene Resource and Molecular Development, College of Life Science, Beijing Normal University, Beijing 100875, China.
Cell Rep. 2025 May 27;44(5):115672. doi: 10.1016/j.celrep.2025.115672. Epub 2025 May 3.
Upon perception of microbe-associated molecular patterns (MAMPs), plants close plasmodesmata (PD) as part of their innate immune responses. However, the signaling cascades and molecular mechanisms underlying MAMP-induced PD closure require further investigation. Here, we show that the endoplasmic reticulum (ER)-plasma membrane (PM) tether Synaptotagmin 1 (Syt1) modulates the response of PD to MAMPs. Following MAMP stimulation, Syt1 rapidly accumulates to PD and further recruits a putative calcium-permeable transporter, ANN4, to promote a localized, PD-associated Ca elevation, leading to callose-dependent PD closure. Moreover, Syt1 can sense the increased level of PI(4,5)P at the PD-PM via its C2 domain. Disrupting the interaction between Syt1 and PM lipids by pharmaceutical approaches or site-directed mutagenesis leads to impaired PD response to MAMPs. Collectively, our findings reveal that Syt1 integrates phospholipid signaling from the PD-PM to regulate PD-localized Ca elevation, thereby modulating intercellular communication for restricting the spread of bacterial infection.
在感知微生物相关分子模式（MAMPs）后，植物会关闭胞间连丝（PD），这是其固有免疫反应的一部分。然而，MAMP诱导的PD关闭背后的信号级联反应和分子机制仍需进一步研究。在这里，我们表明内质网（ER）-质膜（PM）连接蛋白突触结合蛋白1（Syt1）调节PD对MAMPs的反应。在MAMP刺激后，Syt1迅速积累到PD，并进一步招募一种假定的钙通透转运体ANN4，以促进局部的、与PD相关的钙升高，导致胼胝质依赖性PD关闭。此外，Syt1可以通过其C2结构域感知PD-PM处PI(4,5)P水平的升高。通过药物方法或定点诱变破坏Syt1与PM脂质之间的相互作用会导致PD对MAMPs的反应受损。总的来说，我们的研究结果表明，Syt1整合来自PD-PM的磷脂信号，以调节PD处的钙升高，从而调节细胞间通讯，限制细菌感染的传播。
