Evidence map›Paper›PMID 41964446›Full record

ReviewPlant biotechnology journal2026

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

Zhe Meng, Shuqin Zheng, Federica Brandizzi, Yiran Liu, Chunlei Li, Congcong Ai, Yujiao Wang, Jiadong Qi, Xiuguo Zhang

Abstract readReview
In one paragraph

Review in Plant biotechnology journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Zhe MengShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.
Shuqin ZhengShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.
Federica BrandizziPlant Research Laboratory, Michigan State University, East Lansing, Michigan, USA.
Yiran LiuShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.
Chunlei LiShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.
Congcong AiShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.
Yujiao WangShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.
Jiadong QiShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.
Xiuguo ZhangShandong Provincial Key Laboratory of Plant Stress Biology and Genetic Improvement, College of Life Sciences, Shandong Normal University, Jinan, China.

Funding

National Key Research and Development Program of China 2022YFD1401300National Natural Science Foundation of China 32100228
6 · The paper itself

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.

Indexed as

Endoplasmic Reticulum StressHost-Pathogen InteractionsPlant DiseasesPlant ImmunityPlantsSignal TransductionUnfolded Protein Responseeffector‐triggered immunityendoplasmic reticulum stressER‐quality controlpathogen effectorpattern‐triggered immunityplant immunityunfolded protein response

Identifiers

PMID41964446
PMCPMC13387897

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.