TY - JOUR
T1 - Autophagic components contribute to hypersensitive cell death in Arabidopsis
AU - Hofius, Daniel
AU - Schultz-Larsen, Torsten
AU - Joensen, Jan
AU - Tsitsigiannis, Dimitrios I
AU - Petersen, Nikolaj H T
AU - Mattsson, Ole
AU - Jørgensen, Lise Bolt
AU - Jones, Jonathan D G
AU - Mundy, John
AU - Petersen, Morten
N1 - Keywords: Apoptosis; Arabidopsis; Arabidopsis Proteins; Autophagy; DNA-Binding Proteins; Gene Expression Regulation, Plant; Immunity, Innate; Plant Proteins
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
U2 - 10.1016/j.cell.2009.02.036
DO - 10.1016/j.cell.2009.02.036
M3 - Journal article
C2 - 19450522
SN - 0092-8674
VL - 137
SP - 773
EP - 783
JO - Cell
JF - Cell
IS - 4
ER -