Ancient autophagy pathways are emerging as key defense modules in host eukaryotic cells against microbial pathogens. Apart from actively eliminating intracellular intruders, autophagy is also responsible for cell survival, for example by reducing the deleterious effects of endoplasmic reticulum stress. At the same time, autophagy can contribute to cellular suicide. The concurrent engagement of autophagy in these processes during infection may sometimes mask its contribution to differing pro-survival and pro-death decisions. The importance of autophagy in innate immunity in mammals is well documented, but how autophagy contributes to plant innate immunity and cell death is not that clear. A few research reports have appeared recently to shed light on the roles of autophagy in plant-pathogen interactions and in disease-associated host cell death. We present a first attempt to reconcile the results of this research. Cell Death and Differentiation (2011) 18, 1257-1262 doi:10.1038/cdd.2011 published online 29 April 2011 Autophagy mediates the degradation of bulk proteins and is also involved in the clearance of damaged organelles, insoluble protein aggregates and lipids. 1-3 Autophagic digestion and recycling can occur as a survival mechanism to maintain cellular homeostasis and to respond to environmental stresses, such as nutrient depletion or pathogen attack, but may also function as a mediator and/or mechanism of programmed cell death. [4][5][6][7][8] Several subtypes of autophagy are described, but macroautophagy (hereafter termed autophagy) is the most extensively studied 9 and will be the only form described here. The process is characterized by the formation of large, double-membrane vesicles called autophagosomes. These structures arise from expanding single membranes (termed phagophores), which enclose cytoplasmic material and organelles for degradation. Completed autophagosomes fuse with the vacuole/lysosome to release the inner singlemembrane vesicle, called the autophagic body, into the lumen for hydrolytic degradation and recycling. 2,10 The mechanism of autophagy is conserved in yeast, plants and metazoans, and involves the action of canonical autophagy related genes (ATG) that synthesize and coordinate membrane rearrangements to allow cellular catabolism. 1,2 The core sets of ATG genes seem to be present in all eukaryotes and to be essential for the autophagy pathway (Figure 1). For instance, induction of autophagy requires the negative regulator target of rapamycin (TOR) kinase and the ATG1 kinase complex, which control the activity of the phosphatidylinositol 3-kinase complex containing, for example, ATG6/Beclin1. 11 Initiation and completion of autophagosome formation involves two ubiquitin-like conjugation systems to produce ATG12-ATG5 and ATG8-phosphatidylethanolamine (ATG8-PE) conjugates. ATG8-PE conjugation involves the cysteine proteinase ATG4 and the E1-like protein ATG7, and lipidated ATG8 is linked to and translocated with autophagosomes to the vacuole. 12 Therefore, conversion from solu...