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Updated: Apr 13, 2026

Bacterial Leaf Infiltration Assay for Fine Characterization of Plant Defense Responses using the Arabidopsis thaliana-Pseudomonas syringae Pathosystem

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Published on: October 1, 2015

Unfolding Plant Defence: Endoplasmic Reticulum Stress Signalling at the Plant-Pathogen Interface.

Zhe Meng¹, Shuqin Zheng¹, Federica Brandizzi²

¹Shandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.

Plant Biotechnology Journal

|April 11, 2026

Summary

This summary is machine-generated.

Plants harness the endoplasmic reticulum (ER) stress response to fight pathogens, but microbes evolve to evade these defenses. Understanding this ER stress-immune crosstalk is key to enhancing crop resilience.

Keywords:

ER‐quality control effector‐triggered immunity endoplasmic reticulum stress pathogen effector pattern‐triggered immunity plant immunity unfolded protein response

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Area of Science:

Plant Biology
Molecular Plant Pathology
Cellular Proteostasis

Background:

The endoplasmic reticulum (ER) stress response is a crucial proteostasis network in plants.
This network plays a significant role in reprogramming plant immunity against pathogen attacks.

Purpose of the Study:

To synthesize how plants utilize ER stress signaling for defense.
To explore pathogen counterstrategies targeting ER stress pathways.
To delineate the integration of the unfolded protein response (UPR) with plant immune responses.

Main Methods:

Review of existing literature on ER stress and plant immunity.
Analysis of molecular mechanisms integrating UPR with pattern-triggered immunity (PTI) and effector-triggered immunity (ETI).
Examination of salicylic acid (SA) and jasmonic acid (JA) roles in ER stress-immune crosstalk.

Main Results:

UPR enhances plant immunity by regulating protein folding, secretion, transcription, translation, ER-dependent programmed cell death (ER-PCD), ER-associated degradation (ERAD), and autophagy.
Pathogens deploy virulence factors to target UPR components, thereby suppressing ER-driven immunity.
The outcome of UPR activation (resistance vs. susceptibility) depends on pathogen lifestyle, ER stress dynamics, and effector intervention.

Conclusions:

ER stress and immune signaling exhibit a dynamic interplay in plants.
Understanding this crosstalk offers opportunities to improve crop resilience against climate change challenges.
Distinguishing UPR-mediated effects from transgene functions is crucial in biotechnological applications.