Evidence map›Paper›PMID 41389240›Full record

ArticlePlant cell reports2025

ERF3 represses SA pathway defense to modulate tradeoffs between biotic and abiotic stress responses in Arabidopsis.

Ye Fan, Ye Jin, Wannian Yang

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Article in Plant cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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2citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Ye Fan *Key Laboratory of Pesticide and Chemical Biology of Ministry of Education, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, 430079, China.
Ye Jin *Key Laboratory of Pesticide and Chemical Biology of Ministry of Education, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, 430079, China.
Wannian YangKey Laboratory of Pesticide and Chemical Biology of Ministry of Education, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan, 430079, China. yangwn@ccnu.edu.cn.ORCID http://orcid.org/0000-0003-0056-7448

Funding

National Natural Science Foundation of China 31470365
6 · The paper itself

Abstract

key messageAs a repressor of SA pathway, ERF3 is induced by pathogens to repress the expression of SA pathway genes and promote JA-mediated wounding and ABA-mediated abiotic-stress responses in defense response. ERF/AP2 family transcription factors play crucial roles in plant growth, development, and stress responses. However, the function of most family members remains unclear. Here, the role of ERF3 in disease resistance was investigated by transcriptomic sequencing. erf3 mutants are more resistant, whereas ERF3-overexpression (ERF3-OE) plants are more susceptible to bacterial pathogen Pst DC3000 than wild type. Through transcriptomic sequencing, we identified 175 differentially expressed genes (DEGs) between erf3 and wild-type plants, including 44 up-regulated (erf3up) and 131 downregulated genes (erf3down) in erf3. GO analysis showed that erf3up DEGs were most significantly enriched in defense response, including SA pathway marker genes PR2 and PR5, and defense genes RLP23, WRKY53, and RAV2 which play positive roles in resistance against Pst DC3000. By contrast, erf3down DEGs were significantly enriched in response to wounding/jasmonic acid, response to abscisic acid/water deprivation, etc., but no components of JA pathway disease resistance were down-regulated by loss of ERF3 function, indicating ERF3 positively regulate JA-mediated wounding and ABA-mediated abiotic-stress responses upon pathogen infection. ERF3 is induced by Pst DC3000, SA and JA, and ERF3 protein was detected to enrich on PR5 and RAV2 which harbor DRE boxes on the promoter and are up-regulated in erf3 mutants. Overall, ERF3 functions as a repressor in SA pathway disease resistance, and upon pathogen infection, ERF3 is induced to repress the expression of SA pathway genes and promote JA-mediated wounding and ABA-mediated abiotic-stress responses. Our work provides novel insights into the potential of exploiting ERF3 function to enhance plant disease resistance.

Indexed as

ArabidopsisArabidopsis ProteinsSalicylic AcidStress, PhysiologicalTranscription FactorsAbscisic AcidCyclopentanesDisease ResistanceGene Expression Regulation, PlantOxylipinsPlant DiseasesPlants, Genetically ModifiedPseudomonas syringaeSignal TransductionAbscisic AcidArabidopsis ProteinsCyclopentanesjasmonic acidOxylipinsSalicylic AcidTranscription FactorsArabidopsis thalianaDisease resistanceEthylene response factor 3Jasmonic acid pathwayPst DC3000Salicylic acid pathway

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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.