菌体效应器AVRblb2通过传感器准循环核酸通道,以抑制模式触发的免疫力
Soeui Lee1,2, Hye-Young Lee1, Hui Jeong Kang1
1Plant Immunity Research Center, Plant Genomics and Breeding Institute, Seoul National University, Seoul, 08826, Korea.
The New phytologist
|November 28, 2023
概括
植物免疫反应涉及循环核酸通道 (CNGC) 介导的流入. 像AVRblb2这样的病原体作用者利用calmodulin (CaM) 和calmodulin-like (CML) 蛋白来操纵这些通道,以促进感染.
科学领域:
- 植物免疫力 植物免疫力
- 分子植物病原体相互作用
- 信号传递的.
背景情况:
- 过渡性细胞质Ca2+增加对植物病原体相关分子模式 (PAMP) 触发的免疫 (PTI) 至关重要.
- 循环核酸通道 (CNGCs) 调解Ca2+的流入,但它们在PTI中的调节尚不清楚.
- 病原体效应者可以操纵宿主信号通路.
研究的目的:
- 在PTI中阐明NbCNGCs的监管机制.
- 研究calmodulin (CaM) 和calmodulin-like (CML) 蛋白在AVRblb2-NbCNGC相互作用中的作用.
- 了解病原体影响者如何准CNGC来促进感染.
主要方法:
- 同免疫沉测试检测蛋白质复合体的形成.
- 基因沉默以评估NbCNGCs在植物防御和病原体毒性中的作用.
- 在植物病原体相互作用期间分析Ca2+流入动态.
主要成果:
- AVRblb2通过CaM和CML辅因子与NbCNGCs相互作用,形成一个AVRblb2-CaM/CML-NbCNGCs复合体.
- 在PTI期间,CaM和CML通常与NbCNGC18分离,以增加Ca2+的流入,但AVRblb2破坏了这种分离,抑制了通道激活.
- 沉默NbCNGCs损害了AVRblb2的毒性,证实了其针对CNGCs的致病性.
结论:
- AVRblb2通过防止CaM/CML与NbCNGCs分离来抑制PTI诱导的Ca2+流入.
- NbCNGCs形成异构道,为适当的PTI反应微调细胞质Ca2+水平.
- 像AVRblb2这样的病原体作用者利用宿主CNGC和CaM/CML蛋白来操纵宿主免疫力并促进感染.
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