Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis
Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis
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DOI：
10.1016/j.cell.2009.02.036
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发表时间：
2009-05-15
期刊：
影响因子：
64.5
通讯作者：
Petersen, Morten
中科院分区：
文献类型：
--
作者：
Hofius, Daniel;Schultz-Larsen, Torsten;Petersen, Morten
自噬被认为是植物先天免疫过程中的一种促生存机制，可以抑制由病原体引发的过敏反应（HR）引起的程序性细胞死亡（PCD）。该模型基于HR病变在具有降低的自噬基因表达的植物中传播的观察。在这里，我们研究了受体介导的HR PCD反应自噬缺陷的拟南芥基因敲除突变体（ATG），并显示感染诱导的病变包含在ATG突变体。我们还提供了证据表明，HR细胞死亡通过Toll/白细胞介素-1（TIR）型免疫受体通过防御调节因子EDS 1启动，在atg突变体中受到抑制。此外，我们证明了卷曲螺旋（CC）型免疫受体通过NDR 1触发的PCD是自噬独立的或自噬成分与组织蛋白酶和其他未识别的细胞死亡介质。因此，自噬性细胞死亡有助于HR PCD，并且可以与其他促死亡途径平行发挥作用。
Autophagy has been implicated as a prosurvival mechanism to restrict programmed cell death (PCD) associated with the pathogen-triggered hypersensitive response (HR) during plant innate immunity. This model is based on the observation that HR lesions spread in plants with reduced autophagy gene expression. Here, we examined receptor-mediated HR PCD responses in autophagy-deficient Arabidopsis knockout mutants (atg), and show that infection-induced lesions are contained in atg mutants. We also provide evidence that HR cell death initiated via Toll/Interleukin-1 (TIR)-type immune receptors through the defense regulator EDS1 is suppressed in atg mutants. Furthermore, we demonstrate that PCD triggered by coiled-coil (CC)-type immune receptors via NDR1 is either autophagy-independent or engages autophagic components with cathepsins and other unidentified cell death mediators. Thus, autophagic cell death contributes to HR PCD and can function in parallel with other prodeath pathways.