Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA; Department of Biology, Duke University, Durham, NC 27708, USA.
Howard Hughes Medical Institute, Duke University, Durham, NC 27708, USA; Department of Biology, Duke University, Durham, NC 27708, USA.
Curr Opin Immunol. 2022 Apr;75:102169. doi: 10.1016/j.coi.2022.102169. Epub 2022 Feb 12.
Upon pathogen challenge, plant cells can mount defense not only by triggering programmed cell death (PCD) to limit pathogen growth, but also by secreting immune signals to activate subsequent organism-scale defense responses. Recent advances in the study of plant immune mechanisms have found that pathogen-induced oligomerization of immune receptors is a common 'on' switch for the normally self-inhibitory proteins. The resulting 'resistosome' triggers PCD through the formation of a calcium channel or a NADase. Synergy between different receptor-mediated signaling pathways appears to be required for sustained immune induction to trigger PCD of infected cells. In the neighboring cells, PCD is inhibited through the production of immune signal salicylic acid (SA) which mediates degradation of PCD-inducing immune components in biomolecular condensates. Future work is required to connect the resistosome-mediated channel formation and the NADase activity to the downstream regulation of immune execution.
受到病原体攻击时,植物细胞不仅可以通过触发程序性细胞死亡 (PCD) 来限制病原体生长,还可以通过分泌免疫信号来激活后续的全生物体防御反应。最近在植物免疫机制研究方面的进展发现,病原体诱导免疫受体寡聚化是通常自我抑制蛋白的常见“开启”开关。由此产生的“抗性体”通过形成钙通道或 NADase 触发 PCD。不同受体介导的信号通路之间的协同作用似乎是持续免疫诱导以触发受感染细胞的 PCD 所必需的。在相邻细胞中,PCD 被免疫信号水杨酸 (SA) 的产生所抑制,SA 介导生物分子凝聚物中 PCD 诱导免疫成分的降解。需要进一步的工作将抗性体介导的通道形成和 NADase 活性与免疫执行的下游调控联系起来。