Perturbations of the ZED1 pseudokinase activate plant immunity.

Abstract:

:The Pseudomonas syringae acetyltransferase HopZ1a is delivered into host cells by the type III secretion system to promote bacterial growth. However, in the model plant host Arabidopsis thaliana, HopZ1a activity results in an effector-triggered immune response (ETI) that limits bacterial proliferation. HopZ1a-triggered immunity requires the nucleotide-binding, leucine-rich repeat domain (NLR) protein, ZAR1, and the pseudokinase, ZED1. Here we demonstrate that HopZ1a can acetylate members of a family of 'receptor-like cytoplasmic kinases' (RLCK family VII; also known as PBS1-like kinases, or PBLs) and promote their interaction with ZED1 and ZAR1 to form a ZAR1-ZED1-PBL ternary complex. Interactions between ZED1 and PBL kinases are determined by the pseudokinase features of ZED1, and mutants designed to restore ZED1 kinase motifs can (1) bind to PBLs, (2) recruit ZAR1, and (3) trigger ZAR1-dependent immunity in planta, all independently of HopZ1a. A ZED1 mutant that mimics acetylation by HopZ1a also triggers immunity in planta, providing evidence that effector-induced perturbations of ZED1 also activate ZAR1. Overall, our results suggest that interactions between these two RLCK families are promoted by perturbations of structural features that distinguish active from inactive kinase domain conformations. We propose that effector-induced interactions between ZED1/ZRK pseudokinases (RLCK family XII) and PBL kinases (RLCK family VII) provide a sensitive mechanism for detecting perturbations of either kinase family to activate ZAR1-mediated ETI.

journal_name

PLoS Pathog

journal_title

PLoS pathogens

authors

Bastedo DP,Khan M,Martel A,Seto D,Kireeva I,Zhang J,Masud W,Millar D,Lee JY,Lee AH,Gong Y,Santos-Severino A,Guttman DS,Desveaux D

doi

10.1371/journal.ppat.1007900

subject

Has Abstract

pub_date

2019-07-03 00:00:00

pages

e1007900

issue

7

eissn

1553-7366

issn

1553-7374

pii

PPATHOGENS-D-19-00547

journal_volume

15

pub_type

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