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A host–pathogen interactome uncovers phytopathogenic strategies to manipulate plant ABA responses
Author(s) -
Cao Feng Y.,
Khan Madiha,
Taniguchi Masatoshi,
Mirmiran Armand,
Moeder Wolfgang,
Lumba Shelley,
Yoshioka Keiko,
Desveaux Darrell
Publication year - 2019
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.14425
Subject(s) - pseudomonas syringae , abscisic acid , arabidopsis , effector , biology , virulence , transcription factor , microbiology and biotechnology , interactome , pathogen , gene , genetics , mutant
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.