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<p>Global climate change and the rising prevalence of plant pathogens highlight the urgent need for sustainable strategies to enhance plant resilience. Microbial endophytes contribute to stress tolerance, yet their assembly is strongly influenced by host genetics. Here, we examined the roles of <i>Arabidopsis thaliana</i> pectin methylesterases <i>PME12</i> and <i>PME53</i>, key enzymes in cell wall modification under heat stress, in shaping early endophyte colonization and modulating responses to <i>Alternaria alternata</i>, the causal agent of leaf blight. Heat stress promoted the enrichment of specific endophytes such as <i>Rhodococcus ruber</i> At-8, which exhibited strong antagonism toward <i>A. alternata</i> and enhanced seedling resistance, but provided limited protection in mature plants, indicating developmental-stage specificity in host-microbe interactions. Transcript analyses revealed that <i>PME</i>-mediated cell wall remodeling integrates heat and immune signaling by inducing <i>HSFA2</i>, <i>HSP101</i>, <i>HSP18.2</i>,<i> APX2</i>, <i>GSTF8</i>, <i>PR1</i>, and <i>PDF1.2</i>, thereby reinforcing stress adaptation and disease resistance. Collectively, these findings identify <i>PME</i>-dependent cell wall regulation as a pivotal mechanism linking environmental stress tolerance with endophyte-associated immunity.</p>

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Impact of pectin methylesterase on endophyte communities and pathogen resistance in Arabidopsis under heat stress

  • 期刊论文

  • 发表日期：

    2026年2月27日

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  • Jing-Syuan Wang,
  • Pei-Zhen Yang,
  • Hui-Chen Wu

摘要

Global climate change and the rising prevalence of plant pathogens highlight the urgent need for sustainable strategies to enhance plant resilience. Microbial endophytes contribute to stress tolerance, yet their assembly is strongly influenced by host genetics. Here, we examined the roles of Arabidopsis thaliana pectin methylesterases PME12 and PME53, key enzymes in cell wall modification under heat stress, in shaping early endophyte colonization and modulating responses to Alternaria alternata, the causal agent of leaf blight. Heat stress promoted the enrichment of specific endophytes such as Rhodococcus ruber At-8, which exhibited strong antagonism toward A. alternata and enhanced seedling resistance, but provided limited protection in mature plants, indicating developmental-stage specificity in host-microbe interactions. Transcript analyses revealed that PME-mediated cell wall remodeling integrates heat and immune signaling by inducing HSFA2, HSP101, HSP18.2, APX2, GSTF8, PR1, and PDF1.2, thereby reinforcing stress adaptation and disease resistance. Collectively, these findings identify PME-dependent cell wall regulation as a pivotal mechanism linking environmental stress tolerance with endophyte-associated immunity.