Autophagic Components Contribute to Hypersensitive Cell Death in Arabidopsis

作者：Hofius Daniel; Schultz Larsen Torsten; Joensen Jan; Tsitsigiannis Dimitrios I; Petersen Nikolaj H T; Mattsson Ole; Jorgensen Lise Bolt; Jones Jonathan D G; Mundy John; Petersen Morten^*

来源：Cell, 2009, 137(4): 773-783.

DOI：10.1016/j.cell.2009.02.036

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.

• 出版日期2009-5-15