ABSTRACT
KEY MESSAGE: We identify three SDEs that inhibiting host defence from Candidatus Liberibacter asiaticus psy62, which is an important supplement to the pathogenesis of HLB. Candidatus Liberibacter asiaticus (CLas) is the main pathogen of citrus Huanglongbing (HLB). 38 new possible sec-dependent effectors (SDEs) of CLas psy62 were predicted by updated predictor SignalP 5.0, which 12 new SDEs were found using alkaline phosphate assay. Among them, SDE4310, SDE4435 and SDE4955 inhibited hypersensitivity reactions (HR) in Arabidopsis thaliana (Arabidopsis, At) and Nicotiana benthamiana leaves induced by pathogens, which lead to a decrease in cell death and reactive oxygen species (ROS) accumulation. And the expression levels of SDE4310, SDE4435, and SDE4955 genes elevated significantly in mild symptom citrus leaves. When SDE4310, SDE4435 and SDE4955 were overexpressed in Arabidopsis, HR pathway key genes pathogenesis-related 2 (PR2), PR5, nonexpressor of pathogenesis-related 1 (NPR1) and isochorismate synthase 1 (ICS1) expression significantly decreased and the growth of pathogen was greatly increased relative to control with Pst DC3000/AvrRps4 treatment. Our findings also indicated that SDE4310, SDE4435 and SDE4955 interacted with AtCAT3 (catalase 3) and AtGAPA (glyceraldehyde-3-phosphate dehydrogenase A). In conclusion, our results suggest that SDE4310, SDE4435 and SDE4955 are CLas psy62 effector proteins that may have redundant functions. They inhibit ROS burst and cell death by interacting with AtCAT3 and AtGAPA to negatively regulate host defense.
Subject(s)
Arabidopsis , Bacterial Proteins , Nicotiana , Plant Diseases , Reactive Oxygen Species , Arabidopsis/microbiology , Arabidopsis/genetics , Arabidopsis/metabolism , Plant Diseases/microbiology , Nicotiana/genetics , Nicotiana/microbiology , Nicotiana/metabolism , Reactive Oxygen Species/metabolism , Bacterial Proteins/metabolism , Bacterial Proteins/genetics , Plant Leaves/microbiology , Plant Leaves/metabolism , Plant Leaves/genetics , Citrus/microbiology , Citrus/genetics , Citrus/metabolism , Gene Expression Regulation, Plant , Arabidopsis Proteins/metabolism , Arabidopsis Proteins/genetics , Liberibacter/pathogenicity , Liberibacter/physiology , Host-Pathogen Interactions , Plants, Genetically Modified , Plant Proteins/metabolism , Plant Proteins/genetics , Rhizobiaceae/physiology , Disease Resistance/geneticsABSTRACT
In plants, leaf senescence is regulated by several factors, including age and carbon starvation. The molecular mechanism of age-regulated developmental leaf senescence differs from that of carbon starvation-induced senescence. Salicylic acid (SA) and Nonexpressor of pathogenesis-related genes 1 (NPR1) play important roles in promoting developmental leaf senescence. However, the relationship between SA signaling and carbon starvation-induced leaf senescence is not currently well understood. Here, we used Arabidopsis thaliana as material and found that carbon starvation-induced leaf senescence was accelerated in the SA dihydroxylase mutants s3hs5h compared to the Columbia ecotype (Col). Exogenous SA treatment significantly promoted carbon starvation-induced leaf senescence, especially in NPR1-GFP. Increasing the endogenous SA and overexpression of NPR1 inhibited carbon starvation-induced autophagy. However, mutation of NPR1 delayed carbon starvation-induced leaf senescence, increased autophagosome production and accelerated autophagic degradation of the Neighbor of BRCA1 gene 1 (NBR1). In conclusion, SA promotes carbon starvation-induced leaf senescence by inhibiting autophagy via NPR1.