Molecularly Distinct Innexin Gap Junction Channels and Undocked Hemichannels Regulate Glia Morphology and Function in Caenorhabditis elegans
- 1National Centre for Biological Sciences
Abstract
Glial cells across species orchestrate nervous system development, maintenance, and function through ionic and metabolic crosstalk. These cells express multiple gap junction and hemichannel components. However, the mechanisms by which glia communicate utilizing these channel components to support nervous system architecture and function remain poorly understood. By studying GLR glial cells in Caenorhabditis elegans, we show that individual glial cells employ distinct innexin channel configurations to support specific functional roles, utilizing discrete downstream cellular mechanisms. We find that while innexins UNC-7and UNC-9 function as gap junction channels, the innexin INX-18 operates independently to form undocked hemichannels in discrete domains within the same cells. In this combinatorial configuration, UNC-7/UNC-9 gap junctions specifically regulate Synaptobrevin/SNB-1 localization in RME neurons, as previously reported. However, both channel types function non-redundantly to maintain glial morphology by regulating the Calpain/CLP-4 and CDK-5 pathway through cell-autonomous modulation of intracellular calcium levels. In contrast, INX-18 hemichannels in GLR glia regulate high-salt-induced paralysis behavior through distinct downstream cellular mechanisms, potentially in conjunction with tyramine signaling. Altogether, our findings demonstrate a broader repertoire of innexin channel utilization at the individual glial cell level, supporting specific aspects of nervous system maintenance and functioning.
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BibTeX
@misc{sen2026molecularly,
title = {{Molecularly Distinct Innexin Gap Junction Channels and Undocked Hemichannels Regulate Glia Morphology and Function in Caenorhabditis elegans}},
author = {A. Sen and M. X. Mascarenhas and S. Roy and A. Bandyopadhyay and A. Bhattacharya},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.21.753071},
url = {https://www.biorxiv.org/content/10.64898/2026.09.21.753071v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Molecularly Distinct Innexin Gap Junction Channels and Undocked Hemichannels Regulate Glia Morphology and Function in Caenorhabditis elegans
AU - A. Sen
AU - M. X. Mascarenhas
AU - S. Roy
AU - A. Bandyopadhyay
AU - A. Bhattacharya
PY - 2026
DA - 2026/09/21
PB - bioRxiv
DO - 10.64898/2026.09.21.753071
UR - https://www.biorxiv.org/content/10.64898/2026.09.21.753071v1
AB - Glial cells across species orchestrate nervous system development, maintenance, and function through ionic and metabolic crosstalk. These cells express multiple gap junction and hemichannel components. However, the mechanisms by which glia communicate utilizing these channel components to support nervous system architecture and function remain poorly understood. By studying GLR glial cells in Caenorhabditis elegans, we show that individual glial cells employ distinct innexin channel configurations to support specific functional roles, utilizing discrete downstream cellular mechanisms. We find that while innexins UNC-7and UNC-9 function as gap junction channels, the innexin INX-18 operates independently to form undocked hemichannels in discrete domains within the same cells. In this combinatorial configuration, UNC-7/UNC-9 gap junctions specifically regulate Synaptobrevin/SNB-1 localization in RME neurons, as previously reported. However, both channel types function non-redundantly to maintain glial morphology by regulating the Calpain/CLP-4 and CDK-5 pathway through cell-autonomous modulation of intracellular calcium levels. In contrast, INX-18 hemichannels in GLR glia regulate high-salt-induced paralysis behavior through distinct downstream cellular mechanisms, potentially in conjunction with tyramine signaling. Altogether, our findings demonstrate a broader repertoire of innexin channel utilization at the individual glial cell level, supporting specific aspects of nervous system maintenance and functioning.
ER -