Plant diseases caused by pathogens pose a major threat to food security worldwide. A deeper understanding of how plant pathogens cause diseases lays foundations for developing effective strategies to keep plant diseases under control for sustainable agriculture. Many plant pathogens including fungi, bacteria, nematodes, bacteria, and oomycetes rely on effectors that they deliver into plant cells to suppress plant defenses and establish infection. The plant hormone salicylic acid plays an essential role in plant defense against pathogen infection. The investigators discovered that a bacterial type III effector targets the master regulator of salicylic acid-mediated plant defense for degradation, causing disease. This project aims to elucidate the molecular mechanism and biological consequences of the bacterial effector-mediated degradation of the master regulator, and identify a mutant form of the regulator, which cannot be degraded by the effector. This non-degradable regulator could potentially be used to generate disease-resistant plants. Disease-resistant crops are critical to feed a global world population on a decreasing amount of arable land, and to reduce the amount of environmentally harmful pesticides. Two graduate and four undergraduate students will be supported through this project each year. Funding will also be used to train middle school teachers and students in South Carolina to detect citrus greening disease before citrus trees show obvious symptoms in SCienceLab. By connecting hands-on cutting-edge experimentation with urgent real life plant pathology problems, this project will inspire students and make them aware of the importance of plant science.
This project focuses on the targeting of SA-activated NPR1 by the Psudomonas syringae type III effector AvrPtoB. Though it has been known for many years that NPR1 plays an essential role in both local and systemic plant defense, it has not been reported that a pathogen effector targets NPR1. SA facilitates the reduction of plant cytosolic NPR1 oligomers into monomers, which enter the nucleus and function as transcriptional coactivators of plant defense genes. This project showed that SA promotes the interaction between AvrPtoB and NPR1, suggesting that AvrPtoB only interacts with the active form of NPR1. This project demonstrated that AvrPtoB targets NPR1 for degradation, dependent on AvrPtoB's E3 ligase activity. In addition, this project found that the master regulator of SA signaling, NPR1, plays an important role in MTI (MAMP-triggered immunity). This proposal seeks to 1) investigate how SA promotes the interaction between NPR1 and AvrPtoB by determining if AvrPtoB only targets monomeric NPR1 protein, 2) determine the molecular mechanism of AvrPtoB-mediated poly-ubiquitination and degradation of NPR1, 3) show how NPR1 contributes to MTI, and 4) determine how AvrPtoB targets SA-activated NPR1 to disrupt NPR1-dependent MTI to subvert plant innate immunity. These studies will provide fresh insights into effector biology and increase our understanding of MTI and the molecular and biological functions of NPR1 and SA in plant defense. The work will involve training of two postdoctoral fellows to perform research and mentoring of undergraduate students from under-represented groups to empower them to pursue careers in scientific disciplines.
This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.
