一个核心的Plasmopara viticola效应剂减弱了bZIP转录因子的DNA结合活性,从而损害了植物免疫力
Jiaqi Liu1, Tao Ma1, Jianxiang Liang1
1Center for Viticulture and Enology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, 200240, China.
葡萄藤病原体Plasmopara viticola使用效应器PvRXLR13来抑制植物免疫力. 这个效应器针对葡萄的bZIP转录因子,如VvHY5,以促进病原体感染并阻碍葡萄的生产.
科学领域:
- 植物病理学 植物病理学
- 分子植物-微生物相互作用
- 卵菌生物生物学 卵菌生物生物学
背景情况:
- 葡萄藤 (Vitis vinifera L.) 容易受到破坏性的病原体的影响,特别是Plasmopara viticola,它会导致菌.
- 虫病原体分泌效应物来操纵宿主植物的免疫反应,以成功殖民.
研究的目的:
- 确定和描述一种新的Plasmopara viticola效应体,PvRXLR13,参与抑制葡萄藤免疫力.
- 阐明PvRXLR13干扰宿主防御途径的分子机制,特别是涉及bZIP转录因子的途径.
主要方法:
- 来自Plasmopara viticola的PvRXLR13效应物的识别和特征.
- 在葡萄藤和尼科蒂亚娜本塔米亚纳中对PvRXLR13的功能分析,包括抑制ROS,质沉积和细胞死亡.
- 研究PvRXLR13与葡萄树bZIP转录因子VvHY5.5.的相互作用.
- 对VvHY5在植物防护中的作用及其由PvRXLR13.3规范的分析.
主要成果:
- 在P. viticola感染期间诱导PvRXLR13,一个保存的RXLR效应体,并抑制关键的植物免疫反应.
- PvRXLR13抑制ROS积累和病原体触发的细胞死亡,促进葡萄藤和N. benthamiana的殖民.
- 葡萄树bZIP转录因子VvHY5是PvRXLR13的直接目标,它破坏了VvHY5的DNA结合活性和免疫调节功能.
- 过度表达VvHY5增强了对P. viticola的抵抗力,而PvRXLR13通过抑制VvHY5对VvEDS1.1.的激活来对抗这种防御.
结论:
- 葡萄虫使用效应器PvRXLR13通过向bZIP转录因子来解除葡萄藤的免疫系统.
- PvRXLR13破坏了VvHY5介导的防御途径,包括VvEDS1的激活,从而促进了菌体感染.
- 了解这种效应因子-宿主相互作用,可以深入了解虫病原性和葡萄藤疾病耐药性的潜在策略.
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