Autophagy regulates programmed cell death during the plant innate immune response
Autophagy regulates programmed cell death during the plant innate immune response
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DOI：
10.1016/j.cell.2005.03.007
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发表时间：
2005-05-20
期刊：
影响因子：
64.5
通讯作者：
Dinesh-Kumar, SP
中科院分区：
文献类型：
--
作者：
Liu, Y;Schiff, M;Dinesh-Kumar, SP
植物先天免疫反应包括过敏反应（HR），这是一种程序性细胞死亡（PCD）形式。PCD必须局限于感染部位，以防止HR起到病理而非保护作用。在此我们表明，植物的BECLIN 1（酵母和哺乳动物自噬基因ATG6/VPS30/beclin 1的同源物）的作用是将HR PCD限制在感染部位。在缺乏BECLIN 1的植物中，HR PCD的启动是正常的，但值得注意的是，与HR病斑相邻的健康未感染组织以及接种叶片远端的叶片会发生不受限的PCD。在HR PCD反应中，自噬在病原体感染的细胞和远端未感染的细胞中均被诱导；在缺乏BECLIN 1的植物中这种诱导减少。HR PCD的限制还需要其他自噬相关基因的同源物，包括P13K/VPS34、ATG3和ATG7。因此，进化上保守的自噬途径在植物先天免疫中起关键作用，并对PCD起负调控作用。
The plant innate immune response includes the hypersensitive response (HR), a form of programmed cell death (PCD). PCD must be restricted to infection sites to prevent the HR from playing a pathologic rather than protective role. Here we show that plant BECLIN 1, an ortholog of the yeast and mammalian autophagy gene ATG6/VPS30/beclin 1, functions to restrict HR PCD to infection sites. Initiation of HR PCD is normal in BECLIN 1-deficient plants, but remarkably, healthy uninfected tissue adjacent to HR lesions and leaves distal to the inoculated leaf undergo unrestricted PCD. In the HR PCD response, autophagy is induced in both pathogen-infected cells and distal uninfected cells; this is reduced in BECLIN 1-deficient plants. The restriction of HR PCD also requires orthologs of other autophagy-related genes including P13K/VPS34, ATG3, and ATG7. Thus, the evolutionarily conserved autophagy pathway plays an essential role in plant innate immunity and negatively regulates PCD.