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 bluelight 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 proteasomemediated degradation of HRT, likely via COP1, and blue-light relieves this repression resulting in HRT degradation.light | photoreceptors | plant defense | virus | resistance protein P lants are dependent on light for their survival. The light-absorbing ability of plants is derived from the activities of three known classes of photoreceptors. These include phytochromes (PHY) that detect light in the red/far-red (600-700 nm) range, and cryptochromes (CRY) and phototropins (PHOT) that detect light in the blue and UVA (320-500 nm) range (reviewed in refs. 1-6). Photon-absorption activates the PHY proteins from their physiologically inactive to active far-red absorbing forms. Light also modulates the phosphorylation and nucleocytoplasmic translocation of PHY proteins, which is essential for their function in mediating light-responsive physiological changes in plants. CRY photoreceptors are flavoproteins that share sequence similarity to DNA-repair enzymes called photolyases. However, CRY proteins have no DNA-repair activity (5, 7). CRY proteins were first characterized in Arabidopsis, but are also widely distributed in bacteria and eukaryotes. These proteins usually contain an amino terminal photolyase-related region and a carboxy domain of variable size. Both isoforms of CRY (CRY1 and CRY2) in Arabidopsis undergo blue-light-dependent phosphorylation (8, 9), and CRY2, but not CRY1, is degraded in response to blue light (10, 11). Both CRY1 and CRY2 interact with constitutively photomorphogenic 1 (COP1), an E3 ubiquitin ligase (12,13). It is thought that blue-light perception by CRY photoreceptors triggers the rapid inactivation of COP1 through their direct protein-protein interactions (12, 13), resulting in the abrogation of COP1-mediated degradation of the bZIP transcription factor HY5 and other COP1 substrates (14). Although CRY1 protein shuttles between the cytoplasm and nucleus, the CRY2 protein is mostly present in the nucleus (15). Because CRY2 also contributes to anion channel-mediated currents across the plasma membrane (16), it is possible ...

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.glycerol ͉ salicylic acid ͉ stearoyl-acyl carrier protein-desaturase ͉ Turnip Crinkle Virus ͉ ssi2 P lants respond to pathogen perception by triggering a cascade of responses. Perception involves strain-specific detection of a pathogen-encoded elicitor, through direct or indirect interaction, with the corresponding resistance (R) gene product. Such an interaction (also known as incompatible interaction) triggers one or more defense signaling pathways and is often associated with the induction of the hypersensitive response (HR) at the site of pathogen entry. HR is one of the first visible manifestations of the host-induced defense response and is thought to prevent development and movement of the pathogen by inducing deliberate death of the infected cells. R protein-mediated recognition of pathogen can also lead to the accumulation of various phytohormones including salicylic acid (SA), jasmonic acid, and/or ethylene, which in turn signal the activation of defense gene expression. Each hormone activates a specific pathway, and these act individually, synergistically, or antagonistically, depending on the pathogen involved, the ultimate effect of which confers disease resistance and prevents spread of the pathogen to uninoculated parts of the plant.Several components of the SA-mediated pathway have been identified, mutations in which lead to enhanced susceptibility to various pathogens [supporting information (SI...

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Analysis of near-isogenic lines (NILs) indicated the presence of a novel resistance gene in the indica rice cultivar ÔTetepÕ which was highly resistant to the rice blast fungus Magnaporthe grisea. ÔTetepÕ was crossed to the widely used susceptible cultivar ÔCO39Õ to generate the mapping population. A Mendelian segregation ratio of 3 : 1 for resistant to susceptible F 2 plants further confirmed the presence of a major dominant locus, in ÔTetepÕ, conferring resistance to the blast fungal isolate B157, corresponding to the international race IC9. Simple sequence length polymorphism (SSLP) was used for molecular genetic analysis. The analysis revealed that the SSLP marker RM 246 was linked to a novel blast resistance gene designated Pi-tp(t) in ÔTetepÕ.