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<p>Innate immunity is traditionally viewed as a broad defense system with limited specificity. However, increasing evidence suggests that innate immune cells can discriminate between distinct microbial partners. How such specificity arises in early-diverging animals remains unclear. Here, we identify in the sea anemone <i>Nematostella vectensis</i> a selective host innate immune mechanism mediated by nematosomes, motile multicellular bodies that differentially process bacterial cells. Nematosomes preferentially engulf non-native <i>Vibrio</i> isolates while showing reduced uptake of native host-associated strains. We identify the transcription factor cJUN as a key regulator of this process. CRISPR/Cas9-mediated knockout of <i>cJUN</i> reduces nematosome abundance, impairs lysosomal response, alters microbiome assembly, and increases susceptibility to bacterial infection. These results link immune gene function to microbial selectivity and demonstrate that even early-diverging animals exhibit sophisticated innate immunity mechanisms for microbiome regulation. Our findings support the idea that immune specificity can arise through repurposing deeply conserved pathways and may have deep evolutionary origin.</p>

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c-JUN controls microbial colonization via selective phagocytosis in the sea anemone Nematostella

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月10日

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  • N. H. Kaya,
  • M. Abukhalaf,
  • G. Fuentes,
  • J. Taubenheim,
  • U. Hentschel,
  • A. Tholey,
  • S. Fraune

摘要

Innate immunity is traditionally viewed as a broad defense system with limited specificity. However, increasing evidence suggests that innate immune cells can discriminate between distinct microbial partners. How such specificity arises in early-diverging animals remains unclear. Here, we identify in the sea anemone Nematostella vectensis a selective host innate immune mechanism mediated by nematosomes, motile multicellular bodies that differentially process bacterial cells. Nematosomes preferentially engulf non-native Vibrio isolates while showing reduced uptake of native host-associated strains. We identify the transcription factor cJUN as a key regulator of this process. CRISPR/Cas9-mediated knockout of cJUN reduces nematosome abundance, impairs lysosomal response, alters microbiome assembly, and increases susceptibility to bacterial infection. These results link immune gene function to microbial selectivity and demonstrate that even early-diverging animals exhibit sophisticated innate immunity mechanisms for microbiome regulation. Our findings support the idea that immune specificity can arise through repurposing deeply conserved pathways and may have deep evolutionary origin.