Autophagic components contribute to hypersensitive cell death in Arabidopsis.
Autophagy 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 infection-induced 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.
Hofius
Daniel
D
Department of Biology, Copenhagen Biocenter, University of Copenhagen, 2200 Copenhagen, Denmark.
Schultz-Larsen
Torsten
T
Joensen
Jan
J
Tsitsigiannis
Dimitrios I
DI
Petersen
Nikolaj H T
NH
Mattsson
Ole
O
Jørgensen
Lise Bolt
LB
Jones
Jonathan D G
JD
Mundy
John
J
Petersen
Morten
M
D017209:Apoptosis; D017360:Arabidopsis / Q000276:immunology* / Q000378:metabolism; D029681:Arabidopsis Proteins / Q000378:metabolism; D001343:Autophagy; D004268:DNA-Binding Proteins / Q000378:metabolism; D018506:Gene Expression Regulation, Plant; D007113:Immunity, Innate; D010940:Plant Proteins / Q000378:metabolism
D029681:Arabidopsis Proteins; D004268:DNA-Binding Proteins; C118837:EDS1 protein, Arabidopsis; D010940:Plant Proteins; C097421:rps4 protein, plant