NPR1 has been found to be a key transcriptional regulator in some plant defence responses. There are nine We used bioinformatics and reverse genetics approaches to study the expression and function of each We found six members of We discovered a new mode of NPR1 action in wheat at the
Novel Salicylic Acid Analogs Induce a Potent Defense Response in Arabidopsis
The master regulator of salicylic acid (SA)-mediated plant defense, NPR1 (NONEXPRESSER OF PR GENES 1) and its paralogs NPR3 and NPR4, act as SA receptors. After the perception of a pathogen, plant cells produce SA in the chloroplast. In the presence of SA, NPR1 protein is reduced from oligomers to monomers, and translocated into the nucleus. There, NPR1 binds to TGA, TCP, and WRKY transcription factors to induce expression of plant defense genes. A list of compounds structurally similar to SA was generated using ChemMine Tools and its Clustering Toolbox. Several of these analogs can induce SA-mediated defense and inhibit growth of Pseudomonas syringae in Arabidopsis. These analogs, when sprayed on Arabidopsis, can induce the accumulation of the master regulator of plant defense NPR1. In a yeast two-hybrid system, these analogs can strengthen the interactions among NPR proteins. We demonstrated that these analogs can induce the expression of the defense marker gene PR1. Furthermore, we hypothesized that these SA analogs could be potent tools against the citrus greening pathogen Candidatus liberibacter spp. In fact, our results suggest that the SA analogs we tested using Arabidopsis may also be effective for inducing a defense response in citrus. Several SA analogs consistently strengthened the interactions between citrus NPR1 and NPR3 proteins in a yeast two-hybrid system. In future assays, we plan to test whether these analogs avoid degradation by SA hydroxylases from plant pathogens. In future assays, we plan to test whether these analogs avoid degradation by SA hydroxylases from plant pathogens.
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- Award ID(s):
- 1758994
- NSF-PAR ID:
- 10168396
- Date Published:
- Journal Name:
- International Journal of Molecular Sciences
- Volume:
- 20
- Issue:
- 13
- ISSN:
- 1422-0067
- Page Range / eLocation ID:
- 3356
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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Salicylic acid (SA) is a plant defense signal that mediates local and systemic immune responses against pathogen invasion. However, the underlying mechanism of SA-mediated defense is very complex due to the involvement of various positive and negative regulators to fine-tune its signaling in diverse pathosystems. Upon pathogen infections, elevated level of SA promotes massive transcriptional reprogramming in which Non-expresser of PR genes 1 (NPR1) acts as a central hub and transcriptional coactivator in defense responses. Recent findings show that Enhanced Disease Susceptibility 1 (EDS1) also functions as a transcriptional coactivator and stimulates the expression of PR1 in the presence of NPR1 and SA. Furthermore, EDS1 stabilizes NPR1 protein level, while NPR1 sustains EDS1 expression during pathogenic infection. The interaction of NPR1 and EDS1 coactivators initiates transcriptional reprogramming by recruiting cyclin-dependent kinase 8 in the Mediator complex to control immune responses. In this review, we highlight the recent breakthroughs that considerably advance our understanding on how transcriptional coactivators interact with their functional partners to trigger distinct pathways to facilitate immune responses, and how SA accumulation induces dynamic changes in NPR1 structure for transcriptional reprogramming. In addition, the functions of different Mediator subunits in SA-mediated plant immunity are also discussed in light of recent discoveries. Taken together, the available evidence suggests that transcriptional coactivators are essential and potent regulators of plant defense pathways and play crucial roles in coordinating plant immune responses during plant–pathogen interactions.more » « less
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- Free Publicly Accessible Full Text
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Accepted Manuscript1.0
- Journal Article:
- https://doi.org/10.3390/ijms20133356
