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

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

Author information

1
Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520.
2
Department of Biological Sciences, Delaware Biotechnology Institute, University of Delaware, Newark, Delaware 19711.
3
Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032.
4
Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032; Department of Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
5
Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520. Electronic address: savithramma.dinesh-kumar@yale.edu.

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.

PMID:
15907470
DOI:
10.1016/j.cell.2005.03.007
[Indexed for MEDLINE]
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