Inducible cell death in plant immunity

Hofius, Daniel; Tsitsigiannis, Dimitrios Ι.; Jones, Jonathan D. G.; Mundy, John

doi:10.1016/j.semcancer.2006.12.001

Cited by 97 publications

(82 citation statements)

References 284 publications

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“…In contrast to the well-documented signaling pathways associated with HR induction, little is known about how HR cell death is executed, or whether plants share conserved death mechanisms with metazoans (Hofius et al, 2007). The best described form of PCD in animals is apoptosis, but plants apparently lack apoptotic regulatory genes including cysteine proteases called caspases (Lam et al, 2001).…”

Section: Introductionmentioning

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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Section: Introductionmentioning

confidence: 99%

Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis

Hofius¹

2009

Journal of End-to-End-testing

156

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“…One of them is the hypersensitive response, which is often accompanied by programmed cell death, and is effective to prevent the growth of biotrophic pathogens (2). The hypersensitive response is induced coordinately with production of reactive oxygen species, lignification, production of phytoalexins, and expression of defense-related genes.…”

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confidence: 99%

“…Most of lesion mimic mutants are known to activate immune responses in the absence of pathogens (2). A rice lesion mimic mutant, Sekiguchi lesion (sl), exhibits unique orange colored lesions that are induced by inoculation of pathogens, including Magnaporthe grisea (4,5).…”

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confidence: 99%

Sekiguchi Lesion Gene Encodes a Cytochrome P450 Monooxygenase That Catalyzes Conversion of Tryptamine to Serotonin in Rice

Fujiwara

Maisonneuve

Isshiki

et al. 2010

Journal of Biological Chemistry

198

192

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Serotonin is a well known neurotransmitter in mammals and plays an important role in various mental functions in humans. In plants, the serotonin biosynthesis pathway and its function are not well understood. The rice sekiguchi lesion (sl) mutants accumulate tryptamine, a candidate substrate for serotonin biosynthesis. We isolated the SL gene by map-based cloning and found that it encodes CYP71P1 in a cytochrome P450 monooxygenase family. A recombinant SL protein exhibited tryptamine 5-hydroxylase enzyme activity and catalyzed the conversion of tryptamine to serotonin. This pathway is novel and has not been reported in mammals. Expression of SL was induced by the N-acetylchitooligosaccharide (chitin) elicitor and by infection with Magnaporthe grisea, a causal agent for rice blast disease. Exogenously applied serotonin induced defense gene expression and cell death in rice suspension cultures and increased resistance to rice blast infection in plants. We also found that serotonin-induced defense gene expression is mediated by the RacGTPase pathway and by the G␣ subunit of the heterotrimeric G protein. These results suggest that serotonin plays an important role in rice innate immunity.

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“…These results indicated that SA and NADPH oxidases performed a complex interplay in the regulation of cell death. It should be noted that other plant-derived, characterized regulators of cell death, such as jasmonic acid, ethylene (ET), and nitric oxide (NO), seem to be involved in disease development and pathogen resistance as well (Hofius et al, 2007).…”

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confidence: 99%

Dual Roles of Reactive Oxygen Species and NADPH Oxidase RBOHD in an Arabidopsis-Alternaria Pathosystem

et al. 2009

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Arabidopsis (Arabidopsis thaliana) NADPH oxidases have been reported to suppress the spread of pathogen- and salicylic acid-induced cell death. Here, we present dual roles of RBOHD (for respiratory burst oxidase homolog D) in an Arabidopsis-Alternaria pathosystem, suggesting either initiation or prevention of cell death dependent on the distance from pathogen attack. Our data demonstrate that a rbohD knockout mutant exhibits increased spread of cell death at the macroscopic level upon inoculation with the fungus Alternaria brassicicola. However, the cellular patterns of reactive oxygen species accumulation and cell death are fundamentally different in the AtrbohD mutant compared with the wild type. Functional RBOHD causes marked extracellular hydrogen peroxide accumulation as well as cell death in distinct, single cells of A. brassicicola-infected wild-type plants. This single cell response is missing in the AtrbohD mutant, where infection triggers spreading-type necrosis preceded by less distinct chloroplastic hydrogen peroxide accumulation in large clusters of cells. While the salicylic acid analog benzothiadiazole induces the action of RBOHD and the development of cell death in infected tissues, the ethylene inhibitor aminoethoxyvinylglycine inhibits cell death, indicating that both salicylic acid and ethylene positively regulate RBOHD and cell death. Moreover, A. brassicicola-infected AtrbohD plants hyperaccumulate ethylene and free salicylic acid compared with the wild type, suggesting negative feedback regulation of salicylic acid and ethylene by RBOHD. We propose that functional RBOHD triggers death in cells that are damaged by fungal infection but simultaneously inhibits death in neighboring cells through the suppression of free salicylic acid and ethylene levels.

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Inducible cell death in plant immunity

Cited by 97 publications

References 284 publications

Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis

Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis

Sekiguchi Lesion Gene Encodes a Cytochrome P450 Monooxygenase That Catalyzes Conversion of Tryptamine to Serotonin in Rice

Dual Roles of Reactive Oxygen Species and NADPH Oxidase RBOHD in an Arabidopsis-Alternaria Pathosystem

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