Journal
BIOLOGIA PLANTARUM
Volume 59, Issue 3, Pages 570-580Publisher
ACAD SCIENCES CZECH REPUBLIC, INST EXPERIMENTAL BOTANY
DOI: 10.1007/s10535-015-0519-9
Keywords
mutants; pathogen resistance; programmed cell death; Pst-avrRps4
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Funding
- National Natural Science Foundation of China [31170250]
- Natural science Foundation of Guangdong Province [2014A030313420]
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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 DC(3)000 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.
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