Autophagy regulates programmed cell death during the plant innate immune response

被引:1045
作者
Liu, Y
Schiff, M
Czymmek, K
Tallóczy, Z
Levine, B
Dinesh-Kumar, SP [1 ]
机构
[1] Yale Univ, Dept Mol Cellular & Dev Biol, New Haven, CT 06520 USA
[2] Univ Delaware, Delaware Biotechnol Inst, Dept Biol Sci, Newark, DE 19711 USA
[3] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA
[4] Univ Texas, SW Med Ctr, Dept Med, Dallas, TX 75390 USA
关键词
D O I
10.1016/j.cell.2005.03.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
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.
引用
收藏
页码:567 / 577
页数:11
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