Project description:Affymetrix expression analysis was used to validate the role of NPR1 in SA mediated transcription. The RNA of col-0 and npr1-1 mutant were isolated after 24hr water and SA treatment.The ATH1 gene chip was used for expression analysis.
Project description:The plant immune hormone salicylic acid (SA) modulates transcriptional reprogramming via controlling the master transcriptional coactivator, NPR1. Here we examined the role of HECT-type ubiquitin ligases, UPL1 and UPL5, in SA/NPR1-dependent transcriptional control. We showed that UPL1 and UPL5 are essential regulators of SA-responsive genes, and regulate SA-induced transcriptional reprogramming in a NPR1-dependent manner. Four-week old Arabidopsis thaliana plants of wild-type Col-0, mutant upl1, mutant upl5, and mutant npr1-1 genotypes were germinated on soil in 100% relative humidity. Plants were continuously grown in an environmental chamber with 16/8 hour day/night light regime (120 mol m-2 s-1 light intensity), 21/18 degrees celcius day/night cycle and 65% relative humidity. 4-week-old plants were sprayed with water or 0.5 mM SA until all leaves were thoroughly covered with fine droplets, samples were collected after 24 hours treatment. In total two independent biological repeats were collected.
Project description:Wounding is a trigger for both regeneration and defense in plants, but it is not clear if the two responses are linked by common activation or represent potential tradeoffs. While plant glutamate-like receptors (GLRs) are known to mediate defense responses, we implicate GLRs in regeneration through dynamic changes in chromatin and transcription in reprogramming cells near wound sites. Here, we show that genetic mutation and pharmacological inhibition of GLRs increases regeneration efficiency in multiple organ repair systems and plant species. Perturbation of GLR-mediated function, possibly by affecting Calcium fluxes, speeds cell division and re-specification of the stem cell niche while dampening a subset of defense responses. We show that the GLRs work through salicylic acid (SA) signaling in their effects on regeneration, with mutants in the SA receptor NPR1 partially resistant to GLR perturbation and hyper regenerative. These findings reveal a conserved mechanism that regulates a tradeoff between defense and regeneration and also offer new strategies to improve regeneration in agricultural and conservation.
Project description:Nonsteroidal anti-inflammatory drugs (NSAIDs), including salicylic acid (SA), target mammalian cyclooxygenases. In plants, SA is a defense hormone that regulates NON-EXPRESSOR OF PATHOGENESIS RELATED GENES 1 (NPR1), the master transcriptional regulator of immunity-related genes. We identify that the oxicam-type NSAIDs tenoxicam (TNX), meloxicam, and piroxicam, but not other types of NSAIDs, exhibit an inhibitory effect on immunity to bacteria and SA-dependent plant immune response. TNX treatment decreases NPR1 levels, independently from the proposed SA receptors NPR3 and NPR4. Instead, TNX induces oxidation of cytosolic redox status, which is also affected by SA and regulates NPR1 homeostasis. A cysteine labeling assay reveals that cysteine residues in NPR1 can be oxidized in vitro, leading to disulfide-bridged oligomerization of NPR1, but not in vivo regardless of SA or TNX treatment. Therefore, this study indicates that oxicam inhibits NPR1-mediated SA signaling without affecting the redox status of NPR1.
Project description:For over 60 years, salicylic acid (SA) has been known as a plant immune signal required for both basal and systemic acquired resistance (SAR). SA activates these immune responses by reprogramming up to 20% of the transcriptome through the function of NPR1. However, components in the NPR1-signaling hub, which appears as nuclear condensates, and the cascade of the NPR1-signaling pathway remained elusive due to difficulties in studying transcriptional cofactors whose chromosomal associations are often indirect and transient. To overcome this challenge, we applied TurboID to divulge the NPR1-proxiome, which detected key known NPR1-interactors and many new components of transcription-related complexes.
Project description:NPR1 is a central positive regulator of salicylic-acid (SA)-mediated defense signaling in Arabidopsis. Here, we report characterization of OsNPR1, an Oryzae sativa (rice) ortholog of NPR1, focusing on its role in blast disease resistance and identification of OsNPR1-regulated genes followed by their comparison with NPR1-regulated genes in Arabidopsis. Blast resistance tests using OsNPR1–knockdown and –overexpressing rice lines indicated that OsNPR1 plays an essential role in benzothiadiazole-induced blast resistance. Genome-wide transcript profiling using OsNPR1–knockdown lines revealed that 358 genes out of 1,228 BTH-upregulated genes and 724 genes out of 1,069 BTH-downregulated genes were OsNPR1 dependent with respect to their BTH responsiveness, indicating that OsNPR1 plays a major role in the downregulation. Inspection of OsNPR1-dependent genes revealed that many genes involved in photosynthesis and chloroplastic translation and transcription were downregulated by BTH in an OsNPR1 dependent manner, indicating that photosynthesis and chloroplast activities is coordinately suppressed by OsNPR1 in response to BTH-induced activation of SA-signaling pathway. ABA-responsive genes were also OsNPR1-dependently downregulated, suggesting antagonistic interaction of SA signaling on ABA signaling. None of 11 BTH-upregulated genes for WRKY transcription factors was OsNPR1 dependent, whereas most of those are NPR1-dependently upregulated in Arabidopsis, indicating that the role of OsNPR1 is distinct from that of NPR1 in Arabidopsis. We discuss the significance of OsNPR1-regulated gene expression in SA-regulated defense program and the role of OsNPR1 in rice SA-signaling pathway that is branched to OsNPR1- and rice WRKY45-dependent sub-pathways.