Oral: Effector Biology
Degradation of the master regulator of plant defense NPR1 by the type III effector HopAB2
Z. FU (1), H. Chen (1), J. Chen (2), Z. Shang (1), M. Li (1), F. Liu (3) (1) University of South Carolina, U.S.A.; (2) Institute of Plant Protection, Jiangsu Academy of Agricultural Sciences, China; (3) Institute of Plant Protection, Jiangsu Academy of Ag
The plant hormone salicylic acid (SA) is required for systemic acquired resistance (SAR). NPR1, as an SA receptor, is required for SA-mediated plant defense. The expression of over 97% of SA-responsive genes is dependent on NPR1, therefore, NPR1 functions as a master regulator of plant defense. Many studies have shown that pathogen effectors suppress or disrupt MAMP-triggered immunity (MTI) and cell death. There are also isolated studies, which suggest that effectors suppress or disrupt SA-mediated plant defense. In order to provide strong and direct evidence on the targeting of SA-mediated plant defense by pathogen effectors, we tested the interactions between the SA receptor NPR1 and all type III effectors from the bacterial pathogen Pseudomonas syringae in yeast two-hybrid assays. Interestingly, we found that the type III effector HopAB2 interacts with NPR1 only in the presence of SA or its active analogs. Using Agrobacterium co-infiltration assays, we found that HopAB2 degrades GFP- tagged NPR1 protein, dependent on its E3 ligase activity and through the 26S proteasome. Using Dexamethasone (DEX)-inducible Arabidopsis transgenic plants expressing the hopAB2 gene, we found that HopAB2 degrades NPR1 native protein. Similar to npr1-2 mutant plants, these transgenic Arabidopsis plants show sensitivity to SA-induced toxicity and are comprised in SAR. Our studies provide solid evidence that HopAB2 disrupts SA-mediated plant defense by degrading NPR1.