ABSTRACT
Light harvested by plants is essential for the survival of most life forms. This light perception ability requires the activities of proteins termed photoreceptors. We report a function for photoreceptors in mediating resistance (R) protein-derived plant defense. The blue-light photoreceptors, cryptochrome (CRY) 2 and phototropin (PHOT) 2, are required for the stability of the R protein HRT, and thereby resistance to Turnip Crinkle virus (TCV). Exposure to darkness or blue-light induces degradation of CRY2, and in turn HRT, resulting in susceptibility. Overexpression of HRT can compensate for the absence of PHOT2 but not CRY2. HRT does not directly associate with either CRY2 or PHOT2 but does bind the CRY2-/PHOT2-interacting E3 ubiquitin ligase, COP1. Application of the proteasome inhibitor, MG132, prevents blue-light-dependent degradation of HRT, consequently these plants show resistance to TCV under blue-light. We propose that CRY2/PHOT2 negatively regulate the proteasome-mediated degradation of HRT, likely via COP1, and blue-light relieves this repression resulting in HRT degradation.
Subject(s)
Arabidopsis Proteins/metabolism , Cryptochromes/metabolism , Repressor Proteins/metabolism , Ubiquitin-Protein Ligases/metabolism , Arabidopsis/genetics , Arabidopsis/metabolism , Arabidopsis/virology , Arabidopsis Proteins/genetics , Carmovirus/physiology , Cryptochromes/genetics , Gene Expression Profiling , Gene Expression Regulation, Plant , Green Fluorescent Proteins/genetics , Green Fluorescent Proteins/metabolism , Host-Pathogen Interactions , Immunity, Innate/radiation effects , Immunoblotting , Light , Microscopy, Confocal , Mutation , Plant Diseases/genetics , Plant Diseases/virology , Plant Leaves/genetics , Plant Leaves/metabolism , Plant Leaves/virology , Plants, Genetically Modified , Protein Binding , Repressor Proteins/genetics , Reverse Transcriptase Polymerase Chain Reaction , Salicylic Acid/metabolism , Signal Transduction , Ubiquitin-Protein Ligases/geneticsABSTRACT
In Arabidopsis, resistance to Turnip Crinkle Virus (TCV) depends on the resistance (R) gene, HRT, and the recessive locus rrt. Resistance also depends on salicylic acid (SA), EDS1, and PAD4. Exogenous application of SA confers resistance in RRT-containing plants by increasing HRT transcript levels in a PAD4-dependent manner. Here we report that reduction of oleic acid (18:1) can also induce HRT gene expression and confer resistance to TCV. However, the 18:1-regulated pathway is independent of SA, rrt, EDS1, and PAD4. Reducing the levels of 18:1, via a mutation in the SSI2-encoded stearoyl-acyl carrier protein-desaturase, or by exogenous application of glycerol, increased transcript levels of HRT as well as several other R genes. Second-site mutations in the ACT1-encoded glycerol-3-phosphate acyltransferase or GLY1-encoded glycerol-3-phosphate dehydrogenase restored 18:1 levels in HRT ssi2 plants and reestablished a dependence on rrt. Resistance to TCV and HRT gene expression in HRT act1 plants was inducible by SA but not by glycerol, whereas that in HRT pad4 plants was inducible by glycerol but not by SA. The low 18:1-mediated induction of R gene expression was also dependent on ACT1 but independent of EDS1, PAD4, and RAR1. Intriguingly, TCV inoculation did not activate this 18:1-regulated pathway in HRT plants, but instead resulted in the induction of several genes that encode 18:1-synthesizing isozymes. These results suggest that the 18:1-regulated pathway may be specifically targeted during pathogen infection and that altering 18:1 levels may serve as a unique strategy for promoting disease resistance.
