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

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*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

92 Scopus citations

Abstract

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 SCFCOI1 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.

Original languageAmerican English
Pages (from-to)156-168
Number of pages13
JournalCell Host and Microbe
Volume21
Issue number2
DOIs
StatePublished - 8 Feb 2017
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2017 Elsevier Inc.

Keywords

  • HopBB1
  • JAZ
  • Pseudomonas syringae
  • RNA-seq
  • TCP
  • hormone crosstalk
  • jasmonic acid
  • plant immunity
  • sub-nuclear foci
  • virulence effector

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