A Bacterial Effector Co-opts Calmodulin to Target the Plant Microtubule Network

Authors

Ming Guo, University of Nebraska-LincolnFollow
Panya Kim, University of Nebraska–LincolnFollow
Guangyong Li, University of Nebraska-LincolnFollow
Christian Elowsky, University of Nebraska-LincolnFollow
James R. Alfano, University of Nebraska-LincolnFollow

ORCID IDs

Christian Elowsky

Date of this Version

1-12-2016

Citation

Published in Cell Host & Microbe 19, 67–78, January 13, 2016. doi 10.1016/j.chom.2015.12.007

Comments

Copyright © 2016 Elsevier Inc. Used by permission.

Abstract

The bacterial pathogen Pseudomonas syringae depends on effector proteins secreted by its type III secretion system for the pathogenesis of plants. The majority of these effector proteins are known suppressors of immunity, but their plant targets remain elusive. Using Arabidopsis thaliana as a model host, we report that the HopE1 effector uses the host calcium sensor, calmodulin (CaM), as a co-factor to target the microtubule- associated protein 65 (MAP65), an important component of the microtubule network. HopE1 interacted with MAP65 in a CaMdependent manner, resulting in MAP65-GFP dissociation from microtubules. Transgenic Arabidopsis expressing HopE1 had reduced secretion of the immunity protein PR-1 compared to wild–type plants. Additionally, Arabidopsis map65-1 mutants were immune deficient and were more susceptible to P. syringae. Our results suggest a virulence strategy in which a pathogen effector is activated by host calmodulin to target MAP65 and the microtubule network, thereby inhibiting cell wall-based extracellular immunity.

Includes supplementary materials.