Abstract
Psm ES4326/AvrRpt2 (AvrRpt2) was widely used as the reaction system of hypersensitive response (HR) in Arabidopsis. The study showed that in npr1 (GFP-ATG8a), AvrRpt2 was more effective at inducing the production of autophagosome and autophagy flux than that in GFP-ATG8a. The mRNA expression of ATG1, ATG6 and ATG8a were more in npr1 during the early HR. Based on transcriptome data analysis, enhanced disease susceptibility 1 (EDS1) was up-regulated in wild-type (WT) but was not induced in atg4a4b (ATG4 deletion mutant) during AvrRpt2 infection. Compared with WT, atg4a4b had higher expression of salicylic acid glucosyltransferase 1 (SGT1) and isochorismate synthase 1 (ICS1); but less salicylic acid (SA) in normal condition and the same level of free SA during AvrRpt2 infection. These results suggested that the consumption of free SA should be occurred in atg4a4b. AvrRpt2 may trigger the activation of Toll/Interleukin-1 receptor (TIR)-nucleotide binding site (NB)-leucine rich repeat (LRR)—TIR-NB-LRR—to induce autophagy via EDS1, which was inhibited by nonexpressor of PR genes 1 (NPR1). Moreover, high expression of NPR3 in atg4a4b may accelerate the degradation of NPR1 during AvrRpt2 infection.
Highlights
Autophagy is a highly conserved intracellular degradation and recycling procession, which exists in yeast, plants and mammals
ATG knockout mutants display impaired autophagy activity and fail to regulate hypersensitive response (HR)-programmed cell death (PCD) that initiated by Psm ES4326/AvrRpt2 (AvrRpt2) infection [3], which are recognized by Arabidopsis R proteins resistant to Pseudomonas syringae 2 (RPS2) [4]
Toll/Interleukin-1 receptor (TIR)-nucleotide binding site (NB)-leucine rich repeat (LRR) promoted enhanced disease susceptibility 1 (EDS1), which induced autophagy by resistant to P. syringae 4 (RPS4) under AvrRps4 infection; non-race specific disease resistance (NDR1) is required for a different R proteins called coiled-coil (CC)-NB-LRR (CC-NB-LRR), which was mediated by RPS2 under AvrRpt2 infection, and triggers HR independent of autophagy [6]
Summary
Autophagy is a highly conserved intracellular degradation and recycling procession, which exists in yeast, plants and mammals. We explored autophagy induced by AvrRpt during the initial of HR and the new functions of ATG4, related to EDS1. NPR1 functions as a transcriptional activator, whereas NPR3 and NPR4 are transcriptional repressors They all work independently and harmoniously to regulate the expression of downstream genes [12]. Previous work suggested that plant autophagy operated a negative feedback loop modulating SA signaling to negatively regulate senescence and immunity-related PCD [15]. We report that EDS1 is involved in the AvrRpt2-induced autophagy and that ATG4 inhibits the consumption of free SA and alleviates the degradation of NPR1, providing a new insight into the plant autophagy
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