Skip to main content
SLU publication database (SLUpub)
Research article - Peer-reviewed, 2023

The plant trans-Golgi network component ECHIDNA regulates defense, cell death, and endoplasmic reticulum stress

Liu, Lijiang; Qin, Li; Bin Safdar, Luqman; Zhao, Chuanji; Cheng, Xiaohui; Xie, Meili; Zhang, Yi; Gao, Feng; Bai, Zetao; Huang, Junyan; Bhalerao, Rishikesh P.; Liu, Shengyi; Wei, Yangdou

Abstract

The trans-Golgi network component protein ECHIDNA plays important roles in regulating plant immunity and stress responses.The trans-Golgi network (TGN) acts as a central platform for sorting and secreting various cargoes to the cell surface, thus being essential for the full execution of plant immunity. However, the fine-tuned regulation of TGN components in plant defense and stress response has been not fully elucidated. Our study revealed that despite largely compromising penetration resistance, the loss-of-function mutation of the TGN component protein ECHIDNA (ECH) induced enhanced postinvasion resistance to powdery mildew in Arabidopsis thaliana. Genetic and transcriptome analyses and hormone profiling demonstrated that ECH loss resulted in salicylic acid (SA) hyperaccumulation via the ISOCHORISMATE SYNTHASE 1 biosynthesis pathway, thereby constitutively activating SA-dependent innate immunity that was largely responsible for the enhanced postinvasion resistance. Furthermore, the ech mutant displayed accelerated SA-independent spontaneous cell death and constitutive POWDERY MILDEW RESISTANCE 4-mediated callose depositions. In addition, ECH loss led to a chronically prolonged endoplasmic reticulum stress in the ech mutant. These results provide insights into understanding the role of TGN components in the regulation of plant immunity and stress responses.

Published in

Plant Physiology
2023, Volume: 191, number: 1, pages: 558-574
Publisher: OXFORD UNIV PRESS INC

    Associated SLU-program

    SLU Plant Protection Network

    UKÄ Subject classification

    Agricultural Science

    Publication identifier

    DOI: https://doi.org/10.1093/plphys/kiac400

    Permanent link to this page (URI)

    https://res.slu.se/id/publ/119018