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GPR161 mechanosensitivity at the primary cilium drives neuronal saltatory migration
Théo Paillard1,2, Ada Allam1,2, Mohamed Doulazmi1,2
1Sorbonne Université, CNRS, INSERM, NeuroSU, F-75005 Paris, France.
Science Advances
|July 30, 2025
Summary
Neurons use their primary cilia to sense mechanical forces, like fluid shear stress, to guide brain formation. This sensing mechanism, involving GPR161, regulates neuronal migration rhythm.
Area of Science:
- Neuroscience
- Cell Biology
- Biophysics
Background:
- Saltatory neuronal migration is crucial for proper brain development.
- The role of mechanical stimuli in regulating neuronal migration remains largely unexplored.
Purpose of the Study:
- To investigate whether mechanical stimuli, specifically fluid shear stress, regulate neuronal migration.
- To identify the molecular mechanisms underlying mechanosensation during neuronal migration.
Main Methods:
- Utilized an ex vivo neuronal migration model.
- Employed microfluidic assays to apply controlled fluid shear stress.
- Investigated the role of the primary cilium and G protein-coupled receptor 161 (GPR161) using genetic and biochemical approaches.
Main Results:
- Demonstrated that fluid shear stress induces neuronal migration through the primary cilium.
- Identified GPR161, particularly its mechanosensitive helix 8, as a key mechanoreceptor.
- Showed that GPR161 activation triggers a cAMP/PKA signaling pathway, leading to NDE1 phosphorylation and altered microtubule organization, thereby regulating migration.
Conclusions:
- The primary cilium functions as a critical mechanical sensor in neuronal migration.
- Mechanosensation via GPR161 and downstream signaling pathways plays a vital role in regulating the dynamics of neuronal migration for brain formation.
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