自成分有助于阿拉比多普西斯的过敏细胞死亡
Daniel Hofius1, Torsten Schultz-Larsen, Jan Joensen
1Department of Biology, Copenhagen Biocenter, University of Copenhagen, 2200 Copenhagen, Denmark.
Cell
|May 20, 2009
概括
自作为一种生存机制,在病原体防御过程中限制植物细胞死亡. 自缺陷突变体表现出包含的病变,揭示了它在植物免疫期间编程细胞死亡中的作用.
科学领域:
- 植物免疫力 植物免疫力
- 细胞过程是细胞的过程.
- 分子生物学分子生物学
背景情况:
- 自是一种生存机制,在植物天生的免疫过程中限制了编程细胞死亡 (PCD).
- 过敏反应 (HR) 是一种由病原体识别引发的PCD形式.
- 减少自基因表达与HR病变扩散的增加有关.
研究的目的:
- 调查自在受体介导HRPCD中的作用.
- 为了分析自性缺陷的阿拉比多普西斯突变体 (atg) 中的HR反应.
- 确定自与不同免疫受体通路之间的关系.
主要方法:
- 使用了缺少自的阿拉比多普西斯淘汰突变物 (atg).
- 在感染时检查受体介导的HRPCD反应.
- 研究的HR细胞死亡由Toll/Interleukin-1 (TIR) 类型和卷轴-卷轴 (CC) 类型免疫受体触发.
主要成果:
- 感染诱导的HR病变包含在ATG突变体中,与之前的模型相反.
- 由TIR型免疫受体 (通过EDS1) 介导的HR细胞死亡在ATG突变中被抑制.
- 由CC型免疫受体 (通过NDR1) 触发的PCD要么是自独立的,要么是涉及自成分.
结论:
- 自有助于HR PCD,在某些情况下作为一个支持死亡的途径.
- 自细胞死亡可以与植物免疫期间的其他细胞死亡途径并行运行.
- 自在HR PCD中的作用取决于所涉及的特定免疫受体通路.
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