Autophagy and plant innate immunity

Seay, Montrell; Patel, Shalaka; Dinesh‐Kumar, Savithramma P.

doi:10.1111/j.1462-5822.2006.00715.x

Cited by 42 publications

(32 citation statements)

References 45 publications

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“…[38][39][40][41] The results presented in this study provide evidence for the role of autophagy during cell survival. Although there are examples that support the hypothesis of autophagy functioning during cell survival, 12,42 several other studies suggest that autophagy is a pro-death process. 6,42 One possible explanation to reconcile C o p y r i g h t L a n d e s B i o s c i e n c e 2 0 0 8 this difference could be that autophagy may function differently depending on the type of stress involved, the cell type and the developmental stage.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11] At least 36 genes with sequence similarity to the yeast ATG genes are found in the Arabidopsis genome. 8,12 Arabidopsis ATG4 T-DNA knockout mutants are defective in the production of autophagosomes and produce developmentally aberrant roots under nutrient-limiting conditions. 13 In addition, Arabidopsis mutants of ATG7, ATG9 and ATG18a senesce early and are more sensitive to nutrient stress than wild type plants.…”

Section: Introductionmentioning

confidence: 99%

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Arabidopsis ATG6 is required to limit the pathogen-associated cell death response

Patel¹,

2008

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To begin to understand the interplay between autophagy and the hypersensitive response (HR), a type of programmed cell death (PCD) induced during plant innate immunity, we generated ATG6 antisense plants in the genetically tractable Arabidopsis thaliana system. AtATG6 antisense (AtATG6-AS) plants senesce early and are sensitive to nutrient starvation, suggestive of impairment of autophagic function in these plants. Additionally, these plants exhibited multiple developmental abnormalities, a phenomenon not observed in other AtATG mutants. AtATG6-AS plants produced fewer Monodansylcadaverine (MDC) and LysoTracker (LT) stained-autolysosomes in response to carbon and nitrogen starvation indicating that AtATG6 plays a role in the autophagic pathway in Arabidopsis. Interestingly, the level of AtATG6 mRNA in wild type Col-0 Arabidopsis plants is increased during the early phase of virulent and avirulent Pseudomonas syringae pv tomato (Pst) DC3000 infection suggesting that AtATG6 plays an important role during pathogen infection. In AtATG6-AS plants, HR-PCD induced upon infection with avirulent Pst DC3000 carrying the AvrRpm1 effector protein is not able to be contained at the infection site and spreads into uninfected tissue. Additionally, the disease-associated cell death induced by the infection of virulent Pst DC3000 bacteria is also partially misregulated in AtATG6-AS plants. Therefore, the AtATG6 antisense plants characterized here provide an excellent genetic model system to elucidate the molecular mechanisms by which autophagy regulates pathogen-induced cell death.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Arabidopsis ATG6 is required to limit the pathogen-associated cell death response

Patel¹,

2008

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“…In Arabidopsis, autophagy genes are transcriptionally upregulated, but autophagic activity has not been demonstrated upon pathogen infections (Seay et al, 2006;Patel and Dinesh-Kumar, 2008). Therefore, we investigated whether autophagy was also associated with HR cell death in response to bacterial infection in Arabidopsis.…”

Section: Restricted Hr Lesions In Arabidopsis Atg Mutantsmentioning

confidence: 99%

Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis

Hofius¹

2009

Journal of End-to-End-testing

156

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SUMMARYAutophagy has been implicated as a prosurvival mechanism to restrict programmed cell death (PCD) associated with the pathogen-triggered hypersensitive response (HR) during plant innate immunity. This model is based on the observation that HR lesions spread in plants with reduced autophagy gene expression. Here, we examined receptor-mediated HR PCD responses in autophagy-deficient Arabidopsis knockout mutants (atg), and show that infectioninduced lesions are contained in atg mutants. We also provide evidence that HR cell death initiated via Toll/Interleukin-1 (TIR)-type immune receptors through the defense regulator EDS1 is suppressed in atg mutants. Furthermore, we demonstrate that PCD triggered by coiled-coil (CC)-type immune receptors via NDR1 is either autophagy-independent or engages autophagic components with cathepsins and other unidentified cell death mediators. Thus, autophagic cell death contributes to HR PCD and can function in parallel with other prodeath pathways.

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“…Nevertheless, the data led to the hypothesis that autophagy prevents unrestricted HR cell death by yet unknown mechanisms and thus functions as a pro-survival pathway in plant-pathogen interactions. 60,61 More recently, a pro-death function of autophagy during hypersensitive cell death was reported. 62 Here, autophagic activity in the infected tissue accompanied the onset of cell death execution triggered by some, but not all types of R proteins.…”

Section: Autophagy In Plant Immunity and Hypersensitive Cell Deathmentioning

confidence: 99%

Role of autophagy in disease resistance and hypersensitive response-associated cell death

Hofius

Munch²,

Bressendorff³

et al. 2011

Cell Death Differ

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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...

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Autophagy and plant innate immunity

Cited by 42 publications

References 45 publications

Arabidopsis ATG6 is required to limit the pathogen-associated cell death response

Arabidopsis ATG6 is required to limit the pathogen-associated cell death response

Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis

Role of autophagy in disease resistance and hypersensitive response-associated cell death

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