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<p>Glial cells are crucial for nervous system development and function by clearing debris, protecting neurons and ensuring neuronal survival. In <i>Drosophila</i>, glia form the blood–brain barrier, which regulates neural stem cell proliferation and shields the nervous system while maintaining communication with the rest of the organism. To uncover glial-specific roles, we here compare their transcriptome with that of neurons and macrophages. Our study identifies NimA, an uncharacterized member of the Nimrod family, as a glial-specific protein expressed during development. Unlike other family members (i.e. NimC1, Draper and NimC4/Simu) NimA is not involved in phagocytosis. Instead, NimA regulates cell–cell adhesion, crucial for maintaining the tight septate junctions of the larval BBB. Loss of NimA in BBB-forming glia compromises barrier integrity. Moreover, loss of NimA in those glia, or in glia that serve as neural stem cell niche, delays development, reduces brain size, impairs proliferation and reduces the neural stem cell pool. The identification of the glial-specific molecular landscape, including novel molecular players such as NimA, is key for understanding the contribution of glia to the nervous system.</p>

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NimA promotes cell adhesion at the blood brain barrier of the Drosophila nervous system

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月3日

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  • Rosy Sakr,
  • Sara Monticelli,
  • Smrithi Kizhakkenottiyath Shasthadevan,
  • Claude Delaporte,
  • Gege Zhang,
  • Tarek Tabiat,
  • Angela Giangrande,
  • Pierre B Cattenoz

摘要

Glial cells are crucial for nervous system development and function by clearing debris, protecting neurons and ensuring neuronal survival. In Drosophila, glia form the blood–brain barrier, which regulates neural stem cell proliferation and shields the nervous system while maintaining communication with the rest of the organism. To uncover glial-specific roles, we here compare their transcriptome with that of neurons and macrophages. Our study identifies NimA, an uncharacterized member of the Nimrod family, as a glial-specific protein expressed during development. Unlike other family members (i.e. NimC1, Draper and NimC4/Simu) NimA is not involved in phagocytosis. Instead, NimA regulates cell–cell adhesion, crucial for maintaining the tight septate junctions of the larval BBB. Loss of NimA in BBB-forming glia compromises barrier integrity. Moreover, loss of NimA in those glia, or in glia that serve as neural stem cell niche, delays development, reduces brain size, impairs proliferation and reduces the neural stem cell pool. The identification of the glial-specific molecular landscape, including novel molecular players such as NimA, is key for understanding the contribution of glia to the nervous system.