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Key message <p>As 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.</p> Abstract <p>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. <i>erf3</i> mutants are more resistant, whereas <i>ERF3</i>-overexpression (<i>ERF3</i>-OE) plants are more susceptible to bacterial pathogen&#xa0;<i>Pst</i> DC3000 than wild type. Through transcriptomic sequencing, we identified 175 differentially expressed genes (DEGs) between <i>erf3</i> and wild-type plants, including 44 up-regulated (<i>erf3</i>up) and 131 downregulated genes (<i>erf3</i>down) in <i>erf3</i>. GO analysis showed that <i>erf3</i>up DEGs were most significantly enriched in defense response, including SA pathway marker genes <i>PR2</i> and <i>PR5</i>, and defense genes <i>RLP23</i>, <i>WRKY53</i>, and <i>RAV2</i> which play positive roles in resistance against <i>Pst</i> DC3000. By contrast, <i>erf3</i>down 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. <i>ERF3</i> is induced by&#xa0;<i>Pst</i> DC3000, SA and JA, and ERF3 protein was detected to enrich on <i>PR5</i> and <i>RAV2</i> which harbor DRE boxes on the promoter and are up-regulated in <i>erf3</i> mutants. Overall, ERF3 functions as a repressor in SA pathway disease resistance, and upon pathogen infection, <i>ERF3</i> 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.</p>

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

  • 期刊论文

  • 发表日期：

    2025年12月13日

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  • Ye Fan,
  • Ye Jin,
  • Wannian Yang

摘要

Key message

As 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.

Abstract

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.