Biologia Plantarum (Sep 2015)

NADPH oxidase RBOHD contributes to autophagy and hypersensitive cell death during the plant defense response in Arabidopsis thaliana

  • H. B. Liu,
  • X. D. Wang,
  • Y. Y. Zhang,
  • J. J. Dong,
  • C. Ma,
  • W. L. Chen

DOI
https://doi.org/10.1007/s10535-015-0519-9
Journal volume & issue
Vol. 59, no. 3
pp. 570 – 580

Abstract

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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 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.

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