ArticleNeuron2024
Astrocyte growth is driven by the Tre1/S1pr1 phospholipid-binding G protein-coupled receptor.
Article in Neuron, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 22 citations in OpenAlex.
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- An ultrastructural map of a spinal sensorimotor circuit reveals the potential of astroglia modulation.Cell reports · 2026Article
- Regulating glial morphogenesis: insights fromFrontiers in cell and developmental biology · 2026Review
- Glia Preserve Their Own Functions While Compensating for Neighboring Glial Cell Dysfunction.Glia · 2025Article
- Functional profiling and visualization of the sphingolipid metabolic network in vivo.EMBO reports · 2025Article
- Astrocyte Store-Released Calcium Modulates Visual Cortex Synapse Development and Circuit Function.Research square · 2025Article
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- Individual lipid alterations at the origin of neuronal Ceramide Synthase defects.PLoS genetics · 2025Article
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- Glia phagocytose neuronal sphingolipids to infiltrate developing synapses.bioRxiv : the preprint server for biology · 2025Article
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- Glial Regulation of Circuit Wiring, Firing, and Expiring in theCold Spring Harbor perspectives in biology · 2024Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Astrocytes play crucial roles in regulating neural circuit function by forming a dense network of synapse-associated membrane specializations, but signaling pathways regulating astrocyte morphogenesis remain poorly defined. Here, we show the Drosophila lipid-binding G protein-coupled receptor (GPCR) Tre1 is required for astrocytes to establish their intricate morphology in vivo. The lipid phosphate phosphatases Wunen/Wunen2 also regulate astrocyte morphology and, via Tre1, mediate astrocyte-astrocyte competition for growth-promoting lipids. Loss of s1pr1, the functional analog of Tre1 in zebrafish, disrupts astrocyte process elaboration, and live imaging and pharmacology demonstrate that S1pr1 balances proper astrocyte process extension/retraction dynamics during growth. Loss of Tre1 in flies or S1pr1 in zebrafish results in defects in simple assays of motor behavior. Tre1 and S1pr1 are thus potent evolutionarily conserved regulators of the elaboration of astrocyte morphological complexity and, ultimately, astrocyte control of behavior.
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Registered trials
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