The Plant Journal · 2019 · 44 citations · 56 references
AgriculturePlant BiologyPlant SciencesHost-pathogen InteractionsPlant Molecular BiologyPlant-microbe InteractionsPathogen Virulence FactorsPlant Defense ResponsesPlant Hormone SignalingPlant PathogenesisPlant Transcriptional RegulationPlant-pathogen InteractionsAbscisic Acid Response GenesDefense Suppression By Pathogen EffectorsEthylene-responsive Gene ExpressionHormone Signaling In Stress ResponsesMolecular Basis Of VirulencePathogen Response SignalingPlant Pathogen EffectorsPlant Resistance Signaling Pathways
Summary The phytopathogen Pseudomonas syringae delivers into host cells type III secreted effectors (T3 SE s) that promote virulence. One virulence mechanism employed by T3 SE s is to target hormone signaling pathways to perturb hormone homeostasis. The phytohormone abscisic acid ( ABA ) influences interactions between various phytopathogens and their plant hosts, and has been shown to be a target of P. syringae T3 SE s. In order to provide insight into how T3 SE s manipulate ABA responses, we generated an A BA ‐ T 3 SE i nteractome n etwork ( ATIN ) between P. syringae T3 SE s and Arabidopsis proteins encoded by ABA ‐regulated genes. ATIN consists of 476 yeast‐two‐hybrid interactions between 97 Arabidopsis ABA ‐regulated proteins and 56 T3 SE s from four pathovars of P. syringae . We demonstrate that T3 SE interacting proteins are significantly enriched for proteins associated with transcription. In particular, the ETHYLENE RESPONSIVE FACTOR ( ERF ) family of transcription factors is highly represented. We show that ERF 105 and ERF 8 displayed a role in defense against P. syringae , supporting our overall observation that T3 SE s of ATIN converge on proteins that influence plant immunity. In addition, we demonstrate that T3 SE s that interact with a large number of ABA ‐regulated proteins can influence ABA responses. One of these T3 SE s, HopF3 Pph6 , inhibits the function of ERF 8, which influences both ABA ‐responses and plant immunity. These results provide a potential mechanism for how HopF3 Pph6 manipulates ABA ‐responses to promote P. syringae virulence, and also demonstrate the utility of ATIN as a resource to study the ABA ‐T3 SE interface.
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