Biologia plantarum 59:570-580, 2015 | DOI: 10.1007/s10535-015-0519-9
NADPH oxidase RBOHD contributes to autophagy and hypersensitive cell death during the plant defense response in Arabidopsis thaliana
- 1 MOE Key Laboratory of Laser Life Science and Institute of Laser Life Science, College of Biophotonics, South China Normal University, Guangzhou, P.R. China
- 2 Guangdong Key Laboratory of Biotechnology for Plant Development, College of Life Science, South China Normal University, Guangzhou, P.R. China
- 3 Department of Plant Biology and Ecology, College of Life Sciences, Nankai University, Tianjin, P.R. China
Autophagy has been implicated as a cellular protein degradation process that is used to recycle cytoplasmic components under biotic and abiotic stresses and so restrict programmed cell death (PCD). In this study, we report a novel regulatory mechanism by which NADPH oxidase respiratory burst oxidase homolog D (RBOHD) regulated pathogen-induced autophagy and hypersensitive (HR) cell death. We found that the Pseudomonas syringae pv tomato bacteria DC3000 expressing avrRps4 (Pst-avrRps4) induction of RBOHD-dependent reactive oxygen species (ROS) production promoted the onset of autophagy, whereas a pretreatment with an NADPH oxidase RBOHD inhibitor reversed this trend. The inhibitor significantly blocked pathogen-induced autophagosome formation and ROS increase. Moreover, we also show that in the wild-type and atrbohF mutant, Pst-avrRps4-induced cell death was limited, whereas in the case of the atrbohD mutant, the infection triggered a spreading-type necrosis. Our results demonstrate that the RBOHD-dependent ROS accumulation stimulated autophagosome formation and limited HR cell death.
Keywords: mutants; pathogen resistance; programmed cell death; Pst-avrRps4
Subjects: autophagy; hypersensitive reaction; pathogen resistance; NADPH oxidase; mutants; gene expression
Received: July 15, 2014; Revised: January 2, 2015; Accepted: January 8, 2015; Published: September 1, 2015 Show citation
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Supplementary files
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