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Cell. 2009 May 15;137(4):773-83. doi: 10.1016/j.cell.2009.02.036.

Autophagic components contribute to hypersensitive cell death in Arabidopsis.

Author information

1
Department of Biology, Copenhagen Biocenter, University of Copenhagen, 2200 Copenhagen, Denmark.

Abstract

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.

PMID:
19450522
DOI:
10.1016/j.cell.2009.02.036
[Indexed for MEDLINE]
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