Primary cilia mediate specific neuron-glia attachments in C. elegans through the secreted protein BUG-1
4 affiliations
- 1Division of Genetics and Genomics, Boston Children's Hospital, Boston MA 02115 USA
- 2Department of Cell Biology and Neuroscience Institute, New York University School of Medicine, New York NY 10016 USA
- 3Department of Biology, Brandeis University, Waltham MA 02454 USA
- 4Department of Biomedical Sciences, University of Lausanne, 1015 Lausanne Switzerland
Abstract
Primary cilia are signaling hubs that influence nearly every aspect of cell physiology. Neuronal primary cilia were recently found to form extensive attachments to glia in the mammalian brain, but it is not known how these attachments form or what functions they serve. Defects in cilia cause profound neurological disorders, highlighting the importance of understanding the specialized functions of neuronal cilia. Here, we use a genetic screen in Caenorhabditis elegans to determine how a stereotyped cilia-glia attachment forms and how the attachment affects ciliary calcium signaling. We find that two sensory neurons (URX and BAG) use their cilia to attach to a specific glial partner (ILsoL/R). This attachment requires BUG-1, a large secreted protein that localizes precisely to the cilia-glia attachment site. In the absence of BUG-1, neuronal cilia are present but always fail to attach to the glial cell. As a result, the URX cilia do not undergo activity-dependent remodeling seen in wild-type neurons and the BAG cilia exhibit reduced sensory stimulus-evoked calcium entry and defects in calcium clearance. Our work shows that cilia can select specific glial partners for attachment, identifies a novel protein that mediates these attachments, and demonstrates the functional consequences of loss of cilia-glia attachment on neuronal signaling. We propose that neuronal primary cilia act not only as antennae to receive long-range signals but also as points of close-range cell-cell contact, through which glia could modulate neuronal signaling.
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BibTeX
@article{wexler2026primary,
title = {{Primary cilia mediate specific neuron-glia attachments in C. elegans through the secreted protein BUG-1}},
author = {Leland R. Wexler and Brian Griffin and Priya Dutta and Piali Sengupta and Irina Kolotuev and Niels Ringstad and Maxwell G. Heiman},
journal = {Current biology : CB},
year = {2026},
month = oct,
doi = {10.1016/j.cub.2026.10.003},
url = {https://doi.org/10.1016/j.cub.2026.10.003},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Primary cilia mediate specific neuron-glia attachments in C. elegans through the secreted protein BUG-1
AU - Leland R. Wexler
AU - Brian Griffin
AU - Priya Dutta
AU - Piali Sengupta
AU - Irina Kolotuev
AU - Niels Ringstad
AU - Maxwell G. Heiman
PY - 2026
DA - 2026/10/27
JO - Current biology : CB
DO - 10.1016/j.cub.2026.10.003
UR - https://doi.org/10.1016/j.cub.2026.10.003
AB - Primary cilia are signaling hubs that influence nearly every aspect of cell physiology. Neuronal primary cilia were recently found to form extensive attachments to glia in the mammalian brain, but it is not known how these attachments form or what functions they serve. Defects in cilia cause profound neurological disorders, highlighting the importance of understanding the specialized functions of neuronal cilia. Here, we use a genetic screen in Caenorhabditis elegans to determine how a stereotyped cilia-glia attachment forms and how the attachment affects ciliary calcium signaling. We find that two sensory neurons (URX and BAG) use their cilia to attach to a specific glial partner (ILsoL/R). This attachment requires BUG-1, a large secreted protein that localizes precisely to the cilia-glia attachment site. In the absence of BUG-1, neuronal cilia are present but always fail to attach to the glial cell. As a result, the URX cilia do not undergo activity-dependent remodeling seen in wild-type neurons and the BAG cilia exhibit reduced sensory stimulus-evoked calcium entry and defects in calcium clearance. Our work shows that cilia can select specific glial partners for attachment, identifies a novel protein that mediates these attachments, and demonstrates the functional consequences of loss of cilia-glia attachment on neuronal signaling. We propose that neuronal primary cilia act not only as antennae to receive long-range signals but also as points of close-range cell-cell contact, through which glia could modulate neuronal signaling.
SN - 0960-9822
SN - 1879-0445
ER -