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自噬在植物先天免疫反应过程中调节程序性细胞死亡。

Autophagy regulates programmed cell death during the plant innate immune response.

作者信息

Liu Yule, Schiff Michael, Czymmek Kirk, Tallóczy Zsolt, Levine Beth, Dinesh-Kumar S P

机构信息

Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520.

Department of Biological Sciences, Delaware Biotechnology Institute, University of Delaware, Newark, Delaware 19711.

出版信息

Cell. 2005 May 20;121(4):567-577. doi: 10.1016/j.cell.2005.03.007.

Abstract

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 PI3K/VPS34, ATG3, and ATG7. Thus, the evolutionarily conserved autophagy pathway plays an essential role in plant innate immunity and negatively regulates PCD.

摘要

植物先天免疫反应包括超敏反应(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发挥病理作用而非保护作用。在此,我们表明植物中的BECLIN 1是酵母和哺乳动物自噬基因ATG6/VPS30/beclin 1的直系同源物,其功能是将HR PCD局限于感染部位。在缺乏BECLIN 1的植物中,HR PCD的起始是正常的,但值得注意的是,与HR损伤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制的PCD。在HR PCD反应中,病原体感染的细胞和远端未感染的细胞都会诱导自噬;在缺乏BECLIN 1的植物中,这种自噬会减少。HR PCD的局限还需要其他自噬相关基因的直系同源物,包括PI3K/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重要作用,并对PCD起负调控作用。

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