A Pseudomonas syringae type III effector uses calmodulin as co-factor to target the microtubule network
M. GUO (1), P. Kim (2), G. Li (1), C. Elowsky (3), J. Alfano (1) (1) Center for Plant Science Innovation, University of Nebraska-Lincoln, U.S.A.; (2) School of Biological Sciences, University of Nebraska-Lincoln, U.S.A.; (3) Center for Biotechnology, University of Nebraska-Lincoln, U.S.A.

 Pseudomonas syringae uses a type III secretion system to inject proteins known as type III effectors (T3Es) into plants to cause disease. When infected by pathogens, two types of plant immunity can be triggered in plants. Conserved molecules known as pathogen-associated molecular patterns (PAMPs) can be recognized by surface-localized receptors inducing pattern-triggered immunity (PTI). Pathogen effectors can be recognized by specific NOD-like receptors (NLRs) leading to effector-triggered immunity (ETI). The majority of T3Es in P. syringae pv. tomato DC3000 can suppress PTI and/or ETI. The HopE1 T3E contributes to virulence and possesses a robust ability to suppress immunity. We found that HopE1 interacts with the calcium sensor calmodulin (CaM) and HopE1’s ability to bind CaM is required for its contribution to virulence. HopE1 also interacted with MAP65-1, a member of the microtubule-associated protein 65 family. The MAP65-1 and HopE1 interaction was dependent on HopE1’s CaM binding site indicating that HopE1 uses CaM as a cofactor to target MAP65-1. We show that HopE1 dissociates MAP65-1 from the microtubule network. Arabidopsis map65 mutants and plants expressing HopE1 were compromised in PTI, exhibited enhanced susceptibility to P. syringae, and were reduced in the secretion of PR1, an immunity-related protein, suggesting HopE1 inhibits the secretion of immunity-related products to the apoplast and that MAP65 proteins can be components of plant immunity.

Abstract Number: C11-3, P7-224
Session Type: Concurrent