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Autophagy in the control of programmed cell death
Shalaka Patel, Jeffrey Caplan and SP Dinesh-Kumar
Programmed cell death (PCD) is essential for plant development and immunity. Localized PCD is associated with the hypersensitive response (HR), which is a constituent of a successful plant innate immune response. Plants have developed mechanisms to meticulously prevent HR-PCD lesions fromspreading. Our understanding of these mechanisms is still in its incipient stages. A recent study demonstrated that autophagy, a universally conserved process of macromolecule turnover, plays a pivotal role in controlling HR-PCD. The molecular identity of the mediators between the PCD and HR pathways is still obscure, but recent work has begun to shed light on the relationship between HR-PCD andautophagy and to suggest possible mechanisms for the regulation of these pathways.
Addresses Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520-8103, USA Corresponding author: Dinesh-Kumar, SP (

Currently, we know very little about the mechanisms that limit HR-PCD to the initiation site. It is clear that HRPCDthat is induced at the site of infection should be carefully controlled; otherwise, uncontrolled PCD would cause damage to the surrounding uninfected cells. Because plants cells, unlike animal cells, that are undergoing PCD are not removed by phagocytosis, healthy cells need to be protected from toxic materials that might be transported from dying cells. Recent evidence indicates that autophagy thatis induced during the plant innate immune response is one mechanism by which HRPCD is controlled [7]. In this review, we discuss the role of autophagy in HR-PCD and propose possible mechanisms by which autophagy controls HR-PCD.

Autophagy in plants
Autophagy is a process that is conserved across strata and entails the engulfment of cytoplasmic constituents into double-membraned vesiclescalled autophagosomes, which are then targeted to the vacuole or to lysosomes for degradation [8]. Genetic screens in yeast have identified several AuTophaGy (ATG) genes that are required for proper autophagic activity [9]. Even though autophagylike activity has been observed in numerous plant morphological studies over the past three decades, significant progress in understanding autophagic machineryin plants has been made only recently [10,11]. Most of the yeast orthologs of ATG genes are present in plants, and two main approaches have been used to assess the function of these genes: complementation of yeast atg mutants and RNA interference (RNAi) or knockout plants. The Arabidopsis ATG genes AtATG4a/b, AtATG8 and AtATG6/Beclin 1 have been shown to complement their respective yeast deletionstrains by restoring their ability to form autophagosomes or to perform autophagic activity [7,12,13]. The Arabidopsis knockout mutant atg7 has a senescence defect and hypersensitivity to nitrogen and carbon starvation, consistent with a requirement for autophagy during nutrient limitation in yeast and other higher eukaryotes [14]. Autophagy might also play a role in normal plant developmentbecause senescence is accelerated in an Atatg4a/Atatg4b double mutant even under nutrient-rich conditions [12]. Arabidopsis atg3, atg5, atg9 and atg13 mutants have identical developmental phenotypes: accelerated senescence, bolting and reduced seed set [10,11].

Current Opinion in Plant Biology 2006, 9:391–396 This review comes from a themed issue on Biotic interactions Edited by Anne Osbourn andSheng Yang He Available online 19th May 2006 1369-5266/$ – see front matter # 2006 Elsevier Ltd. All rights reserved. DOI 10.1016/j.pbi.2006.05.007

Programmed cell death (PCD) plays an important role during development, senescence and immunity in multicellular organisms [1,2]. The most extensively studied form of plant PCD is the hypersensitive response (HR) to pathogen infection...