TY - JOUR
T1 - A Bacterial Effector Co-opts Calmodulin to Target the Plant Microtubule Network
AU - Guo, Ming
AU - Kim, Panya
AU - Li, Guangyong
AU - Elowsky, Christian G.
AU - Alfano, James R.
N1 - Funding Information:
We thank members of the Alfano laboratory for fruitful discussions on the experiments described in this paper and E. Banset for editing. We thank Drs. J. Dangl for the Arabidopsis yeast two-hybrid cDNA library; S. Shaw for Arabidopsis map65-1 , map65-2 , and map65-1 map65-2 mutants; H. Jin and X. Dong for anti-PR-1 antibodies; D. Desveaux for Arabidopsis MAP4-GFP and EB1-GFP seed; and S. Robatzek for Arabidopsis MAP4-GFP, TUA6-GFP, and TUB6-GFP seed. This research was supported by a University of Nebraska internal grant and a grant from the Nebraska Soybean Board.
Publisher Copyright:
© 2016 Elsevier Inc.
PY - 2016/1/13
Y1 - 2016/1/13
N2 - 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 CaM-dependent 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.
AB - 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 CaM-dependent 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.
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U2 - 10.1016/j.chom.2015.12.007
DO - 10.1016/j.chom.2015.12.007
M3 - Article
C2 - 26764598
AN - SCOPUS:84959479505
SN - 1931-3128
VL - 19
SP - 67
EP - 78
JO - Cell Host and Microbe
JF - Cell Host and Microbe
IS - 1
ER -