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<p>Psyllid-transmitted <i>Candidatus</i> Liberibacter asiaticus (<i>C</i>Las) is a phloem-limited unculturable bacterium that causes citrus Huanglongbing. To date, the mechanisms by which psyllids recognize and respond to this pathogen remain poorly understood. Here, we show that the psyllid Toll8 receptor acts as a pattern recognition receptor for the <i>C</i>Las outer membrane protein Barrel, resulting in Toll8 dimerization and activation. Activated Toll8 subsequently triggers an intracellular signaling cascade, involving MyD88 dimerization and the activation of IκB kinase IKKE, that culminates in the transcriptional activation of the transcription factor NFAT and the expression of antimicrobial effectors. Moreover, we show that <i>C</i>Las counters this immune response by secreting the effector protein SDE3230, which hijacks an E3 ligase to mediate the ubiquitination and degradation of MyD88, thereby suppressing Toll signaling. Our findings define a Toll8-MyD88-IKKE-NFAT immune signaling axis in arthropods and highlight an intricate counter-defense strategy employed by pathogens for survival and propagation within insect vectors.</p>

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The insect Toll pathway activates antibacterial immunity against the citrus Huanglongbing pathogen

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月23日

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  • Yu Du,
  • Mengle Sun,
  • Yuqing Xiao,
  • Jinhua Yang,
  • Manman Hu,
  • Qian Chen,
  • You Li,
  • Taiyun Wei

摘要

Psyllid-transmitted Candidatus Liberibacter asiaticus (CLas) is a phloem-limited unculturable bacterium that causes citrus Huanglongbing. To date, the mechanisms by which psyllids recognize and respond to this pathogen remain poorly understood. Here, we show that the psyllid Toll8 receptor acts as a pattern recognition receptor for the CLas outer membrane protein Barrel, resulting in Toll8 dimerization and activation. Activated Toll8 subsequently triggers an intracellular signaling cascade, involving MyD88 dimerization and the activation of IκB kinase IKKE, that culminates in the transcriptional activation of the transcription factor NFAT and the expression of antimicrobial effectors. Moreover, we show that CLas counters this immune response by secreting the effector protein SDE3230, which hijacks an E3 ligase to mediate the ubiquitination and degradation of MyD88, thereby suppressing Toll signaling. Our findings define a Toll8-MyD88-IKKE-NFAT immune signaling axis in arthropods and highlight an intricate counter-defense strategy employed by pathogens for survival and propagation within insect vectors.