Recognition and Response in the Plant Immune System

Nimchuk, Zachary L.; Eulgem, Thomas; Holt, Ben F.; Dangl, Jeffery L.

doi:10.1146/annurev.genet.37.110801.142628

Cited by 510 publications

(342 citation statements)

References 197 publications

(202 reference statements)

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“…Pathogenic microorganisms of plants are known to secrete proteins directly into host plant cells to perturb host cell signalling or suppress the plant innate immune system 27,28 . The plant adaptive immune system has, in turn, evolved to recognize pathogen effector proteins (often termed pathogen-associated molecular patterns, PAMPs).…”

Section: Fungal Effectors and Pampsmentioning

confidence: 99%

The genome sequence of the rice blast fungus Magnaporthe grisea

Dean

Talbot

Ebbole

et al. 2005

Nature

1,502

1,194

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Magnaporthe grisea is the most destructive pathogen of rice worldwide and the principal model organism for elucidating the molecular basis of fungal disease of plants. Here, we report the draft sequence of the M. grisea genome. Analysis of the gene set provides an insight into the adaptations required by a fungus to cause disease. The genome encodes a large and diverse set of secreted proteins, including those defined by unusual carbohydrate-binding domains. This fungus also possesses an expanded family of G-protein-coupled receptors, several new virulence-associated genes and large suites of enzymes involved in secondary metabolism. Consistent with a role in fungal pathogenesis, the expression of several of these genes is upregulated during the early stages of infection-related development. The M. grisea genome has been subject to invasion and proliferation of active transposable elements, reflecting the clonal nature of this fungus imposed by widespread rice cultivation.Outbreaks of rice blast disease are a serious and recurrent problem in all rice-growing regions of the world, and the disease is extremely difficult to control 1,2 . Rice blast, caused by the fungus Magnaporthe grisea, is therefore a significant economic and humanitarian problem. It is estimated that each year enough rice is destroyed by rice blast disease to feed 60 million people 3 . The life cycle of the rice blast fungus is shown in Fig. 1. Infections occur when fungal spores land and attach themselves to leaves using a special adhesive released from the tip of each spore 4 . The germinating spore develops an appressorium-a specialized infection cell-which generates enormous turgor pressure (up to 8 MPa) that ruptures the leaf cuticle, allowing invasion of the underlying leaf tissue 5,6 . Subsequent colonization of the leaf produces disease lesions from which the fungus sporulates and spreads to new plants. When rice blast infects young rice seedlings, whole plants often die, whereas spread of the disease to the stems, nodes or panicle of older plants results in nearly total loss of the rice grain 2 . Different host-limited forms of M. grisea also infect a broad range of grass species including wheat, barley and millet. Recent reports have shown that the fungus has the capacity to infect plant roots 7 .Here we present our preliminary analysis of the draft genome sequence of M. grisea, which has emerged as a model system for understanding plant-microbe interactions because of both its economic significance and genetic tractability 1,2 . Acquisition of the M. grisea genome sequenceThe genome of a rice pathogenic strain of M. grisea, 70-15, was sequenced through a whole-genome shotgun approach. In all, greater than sevenfold sequence coverage was produced, and a summary of the principal genome sequence data is provided in Table 1 and Supplementary Table S1. The draft genome sequence consists of 2,273 sequence contigs longer than 2 kilobases (kb), ordered and orientated within 159 scaffolds. The total length of all sequence contigs is 38.8 mega...

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Section: Fungal Effectors and Pampsmentioning

confidence: 99%

The genome sequence of the rice blast fungus Magnaporthe grisea

Dean

Talbot

Ebbole

et al. 2005

Nature

1,502

1,194

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“…These R-mediated defenses often include a localized programmed cell death reaction known as the hypersensitive response (HR) to limit pathogen spread. 58 Several examples of the involvement of autophagy in plant immunity and hypersensitive-related cell death have emerged Figure 2 Examples of cell death that depend on autophagy components in different eukaryotic models. In the rice blast fungus Magnaporthe oryzae, autophagic cell death is required for degradation of conidia and thus fungal pathogenicity, which can be inhibited by knockout of ATG8.…”

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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“…However, the further growth of the inappropriate fungus is terminated in each pen mutant coincident with a cell death response of attacked epidermal cells. This cell death is reminiscent of the hypersensitive reaction (HR), which is triggered upon recognition of strain-specific pathogen effectors by race-specific resistance genes [23]. It remains to be tested whether the cell death in pen mutants responding to Bgh is mechanistically similar or dissimilar to the HR.…”

Section: Snare Proteins and The First Line Of Defence Against Fungal mentioning

confidence: 99%

Knocking on the heaven’s wall: pathogenesis of and resistance to biotrophic fungi at the cell wall

Schulze‐Lefert

2004

Current Opinion in Plant Biology

124

101

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New findings challenge the traditional view of the plant cell wall as passive structural barrier to invasion by fungal microorganisms. A surveillance system for cell wall integrity appears to sense perturbation of the cell wall structure upon fungal attack and is interconnected with known plant defence signalling pathways. Biotrophic fungi might manipulate this surveillance system for the establishment of biotrophy. The attempts of fungi to invade also induce a sub-cellular polarisation in attacked cells, which activates an ancient vesicle-associated resistance response that possibly enables the focal transport of regulatory cargo and the secretion of toxic cargo. The underlying resistance machinery might have been subverted by biotrophic fungi for pathogenesis. IntroductionPenetration through the plant cell wall represents an Achilles heel in the pathogenesis of most biotrophic fungi and marks a lifestyle transition from extra-cellular to invasive growth. Modification of the plant cell wall was recognised for the first time as potential resistance mechanism almost 80 years ago following work in which 78 plant species and varieties were challenged with Alternaria spp. and other leaf-spotting fungi [1]. The termination of fungal pathogenesis at the cell wall was commonly associated with wall 'thickenings' and the formation of local additions or 'callosities' in the paramural space (i.e. the space between the cell wall and the plasma membrane). Formation of these cell wall appositions (CWAs) or papillae is usually accompanied by a co-localised accumulation of phenolics and reactive oxygen species [2][3][4][5][6]. The complex process of sub-cellular cell wall remodelling is tightly linked to the rapid disassembly and subsequent focal reassembly of the plant cytoskeleton at fungal entry sites, which is indicative of a pathogen-triggered cell polarisation [6][7][8][9]. There has been a long-standing controversy, however, over whether CWAs function in disease resistance or facilitate the entry of fungal pathogens into host cells by providing a structural collar for the intruder. New molecular genetic data from Arabidopsis and barley have indeed revealed that molecular processes at and in CWAs have Janus-faced functions, that is, functions for fungal pathogenesis and in resistance responses. Focal vesicle transport and vesicle fusion events that are dependent on SNAP (soluble N-ethylmaleimide-sensitive-factor-association protein) receptor (SNARE) proteins at the plasma membrane emerge as potential common underlying mechanisms that might be interconnected with a poorly understood cell wall integrity surveillance system. In this review, I discuss the seemingly paradoxical functions of these processes in establishing the biotrophic lifestyle and in disease resistance at the cell periphery.Linking cell wall structure to biotic stress signalling Callose, a (1!3)-b-D-glucan, has long been known to be synthesised and deposited rapidly at CWAs upon microbial attack. This polymer was thought to contribute to a physical barrie...

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Recognition and Response in the Plant Immune System

Cited by 510 publications

References 197 publications

The genome sequence of the rice blast fungus Magnaporthe grisea

The genome sequence of the rice blast fungus Magnaporthe grisea

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

Knocking on the heaven’s wall: pathogenesis of and resistance to biotrophic fungi at the cell wall

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