ABSTRACT The endoplasmic reticulum (ER) stress response, a conserved proteostasis network, has emerged as a central hub that reprograms plant immunity during pathogen attack. This review synthesises how plants harness ER‐stress signalling to mount multilayered defences and how pathogens have evolved counterstrategies to subvert these pathways. We delineate the molecular integration of the unfolded protein response (UPR) with canonical immune layers including pattern‐triggered immunity (PTI), effector‐triggered immunity (ETI) and systemic defences, highlighting salicylic acid (SA) and jasmonic acid (JA) as rheostats that fine‐tune ER stress‐immune crosstalk. Functionally, the UPR bolsters immunity by coordinating protein folding and secretion, reprogramming transcription and translation, activating ER‐dependent programmed cell death (ER‐PCD), and orchestrating ER‐associated degradation (ERAD) and selective autophagy. Pathogens such as bacteria, oomycetes and viruses in turn deploy virulence factors that target UPR sensors and transcription factors, thereby attenuating ER‐driven immunity. We propose a conceptual framework in which the outcome of UPR activation—resistance versus susceptibility—is determined by pathogen lifestyle, ER stress dynamics, subcellular compartmentalisation and pathogen effector intervention. We also consider biotechnological contexts in which strong transgene expression can itself provoke the UPR, and outline diagnostic experimental strategies to distinguish UPR‐mediated effects from intended transgene functions. By integrating molecular mechanisms with pathogen counterstrategies, this review underscores the dynamic interplay between ER stress and immune signalling in plants and highlights opportunities to enhance crop resilience under global climate challenges.
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zhe meng
Shuqin Zheng
Federica Brandizzi
Plant Biotechnology Journal
Michigan State University
Shandong Normal University
Shandong Agricultural University
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meng et al. (Sat,) studied this question.
www.synapsesocial.com/papers/69dc89183afacbeac03eade4 — DOI: https://doi.org/10.1111/pbi.70662
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