학술논문

Autophagy Regulates Programmed Cell Death during the Plant Innate Immune Response
Document Type
Report
Source
Cell. May 20, 2005, Vol. 121 Issue 4, p567, 11 p.
Subject
Biochemistry
Apoptosis
Developmental biology
Biological sciences
Language
English
ISSN
0092-8674
Abstract
To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.03.007 Byline: Yule Liu (1), Michael Schiff (1), Kirk Czymmek (2), Zsolt Talloczy (3), Beth Levine (3)(4), S.P. Dinesh-Kumar (1) 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. Author Affiliation: (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, University of Texas Southwestern Medical Center, Dallas, Texas 75390 Article Note: (miscellaneous) Published: May 19, 2005