Skip to main navigation Skip to search Skip to main content

The Arabidopsis E3 ubiquitin ligase PUB4 regulates BIK1 and is targeted by a bacterial type-III effector

  • Gang Yu
  • , Maria Derkacheva
  • , Jose S. Rufian
  • , Carla Brillada
  • , Kathrin Kowarschik
  • , Shushu Jiang
  • , Paul Derbyshire
  • , Miaomiao Ma
  • , Thomas A. Defalco
  • , Rafael J. L. Morcillo
  • , Lena Stransfeld
  • , Yali Wei
  • , Jian‐Min Zhou
  • , Frank L. H. Menke
  • , Marco Trujillo
  • , Cyril Zipfel
  • , Alberto P. Macho

Research output: Contribution to journalArticlepeer-review

71 Citations (Scopus)

Abstract

Plant immunity is tightly controlled by a complex and dynamic regulatory network, which ensures optimal activation upon detection of potential pathogens. Accordingly, each component of this network is a potential target for manipulation by pathogens. Here, we report that RipAC, a type III-secreted effector from the bacterial pathogen Ralstonia solanacearum, targets the plant E3 ubiquitin ligase PUB4 to inhibit pattern-triggered immunity (PTI). PUB4 plays a positive role in PTI by regulating the homeostasis of the central immune kinase BIK1. Before PAMP perception, PUB4 promotes the degradation of non-activated BIK1, while after PAMP perception, PUB4 contributes to the accumulation of activated BIK1. RipAC leads to BIK1 degradation, which correlates with its PTI-inhibitory activity. RipAC causes a reduction in pathogen-associated molecular pattern (PAMP)-induced PUB4 accumulation and phosphorylation. Our results shed light on the role played by PUB4 in immune regulation, and illustrate an indirect targeting of the immune signalling hub BIK1 by a bacterial effector.
Original languageEnglish
Article numbere107257
JournalThe EMBO Journal
Volume41
Issue number23
Early online date31 Oct 2022
DOIs
Publication statusPublished - 1 Dec 2022

Keywords

  • BIK1
  • PAMP-triggered immunity
  • PUB4
  • Ralstonia solanacearum
  • phosphorylation

Cite this