Cell death control: the interplay of apoptosis and autophagy in the pathogenicity of Sclerotinia sclerotiorum

Programmed cell death is characterized by a cascade of tightly controlled events that culminate in the orchestrated death of the cell. In multicellular organisms autophagy and apoptosis are recognized as two principal means by which these genetically determined cell deaths occur. During plant-microb...

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Bibliographic Details
Published in:PLoS pathogens 2013-04, Vol.9 (4), p.e1003287
Main Authors: Kabbage, Mehdi, Williams, Brett, Dickman, Martin B
Format: Article
Language:English
Subjects:
Acids
Adenine - analogs & derivatives
Adenine - pharmacology
Androstadienes - pharmacology
Antifungal Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Apoptosis - genetics
Arabidopsis - microbiology
Ascomycota
Ascomycota - genetics
Ascomycota - metabolism
Ascomycota - pathogenicity
Autophagy
Autophagy - drug effects
Autophagy - genetics
Biology
Cameras
Cell death
Cells
Cellular control mechanisms
Chloroquine - pharmacology
Chromones - pharmacology
Fungi
Genetic aspects
Genetics
Genotype & phenotype
Host-Pathogen Interactions
Immunization
Leaves
Mammals
Morpholines - pharmacology
Mycoses
Observations
Organisms
Oxalic Acid - metabolism
Plant Diseases - microbiology
Plant-pathogen relationships
Reactive Oxygen Species
Respiratory Burst - genetics
Software
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Summary:Programmed cell death is characterized by a cascade of tightly controlled events that culminate in the orchestrated death of the cell. In multicellular organisms autophagy and apoptosis are recognized as two principal means by which these genetically determined cell deaths occur. During plant-microbe interactions cell death programs can mediate both resistant and susceptible events. Via oxalic acid (OA), the necrotrophic phytopathogen Sclerotinia sclerotiorum hijacks host pathways and induces cell death in host plant tissue resulting in hallmark apoptotic features in a time and dose dependent manner. OA-deficient mutants are non-pathogenic and trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive response including callose deposition and a pronounced oxidative burst, suggesting the plant can recognize and in this case respond, defensively. The details of this plant directed restrictive cell death associated with OA deficient mutants is the focus of this work. Using a combination of electron and fluorescence microscopy, chemical effectors and reverse genetics, we show that this restricted cell death is autophagic. Inhibition of autophagy rescued the non-pathogenic mutant phenotype. These findings indicate that autophagy is a defense response in this necrotrophic fungus/plant interaction and suggest a novel function associated with OA; namely, the suppression of autophagy. These data suggest that not all cell deaths are equivalent, and though programmed cell death occurs in both situations, the outcome is predicated on who is in control of the cell death machinery. Based on our data, we suggest that it is not cell death per se that dictates the outcome of certain plant-microbe interactions, but the manner by which cell death occurs that is crucial.
ISSN:1553-7374
1553-7366
1553-7374
DOI:10.1371/journal.ppat.1003287