A host–pathogen interactome uncovers phytopathogenic strategies to manipulate plant <scp>ABA</scp> responses

Feng Cao, Madiha Khan, Masatoshi Taniguchi, Armand Mirmiran, Wolfgang Moeder, Shelley Lumba, Keiko Yoshioka, Darrell Desveaux

The Plant Journal · 2019 · 44 citations · 56 references

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Abstract

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.

References

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