Pseudomonas syringae Type III Effector HopBB1 Promotes Host Transcriptional Repressor Degradation to Regulate Phytohormone Responses and Virulence

Publication date: Available online 26 January 2017
Source:Cell Host & Microbe
Author(s): Li Yang, Paulo José Pereira Lima Teixeira, Surojit Biswas, Omri M. Finkel, Yijian He, Isai Salas-Gonzalez, Marie E. English, Petra Epple, Piotr Mieczkowski, Jeffery L. Dangl
Independently evolved pathogen effectors from three branches of life (ascomycete, eubacteria, and oomycete) converge onto the Arabidopsis TCP14 transcription factor to manipulate host defense. However, the mechanistic basis for defense control via TCP14 regulation is unknown. We demonstrate that TCP14 regulates the plant immune system by transcriptionally repressing a subset of the jasmonic acid (JA) hormone signaling outputs. A previously unstudied Pseudomonas syringae (Psy) type III effector, HopBB1, interacts with TCP14 and targets it to the SCF^COI1 degradation complex by connecting it to the JA signaling repressor JAZ3. Consequently, HopBB1 de-represses the TCP14-regulated subset of JA response genes and promotes pathogen virulence. Thus, HopBB1 fine-tunes host phytohormone crosstalk by precisely manipulating part of the JA regulon to avoid pleiotropic host responses while promoting pathogen proliferation.

Graphical abstract

Teaser

Yang et al. demonstrate that the Pseudomonas syringae type III effector HopBB1 modulates two negative regulators of plant jasmonic acid (JA) signaling, TCP14 and JAZ3, and "glues" them together for degradation, resulting in precise activation of a subset of JA output responses that promote bacterial virulence.


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