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Ex Utero Electroporation and Organotypic Slice Cultures of Embryonic Mouse Brains for Live-Imaging of Migrating GABAergic Interneurons
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JNK Signaling Regulates Cellular Mechanics of Cortical Interneuron Migration
Skye E Smith1,2,3, Nicholas K Coker1, Eric S Tucker4,3
1Department of Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506.
Eneuro
|August 2, 2020
Summary
The c-Jun NH2-terminal kinase (JNK) pathway is crucial for guiding inhibitory interneuron migration in the brain. Disrupting JNK signaling impairs key cellular processes, impacting cortical development and potentially leading to neurological disorders.
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- Aberrant migration of inhibitory interneurons contributes to neurological disorders like epilepsy, autism, and schizophrenia.
- The precise mechanisms governing interneuron migration are not fully understood.
Purpose of the Study:
- To investigate the role of the c-Jun NH2-terminal kinase (JNK) pathway in coordinating leading process branching and nucleokinesis during cortical interneuron migration.
Main Methods:
- Live-cell confocal microscopy in a mouse model.
- Pharmacological inhibition of JNK signaling.
- Genetic deletion of JNK in interneurons.
Main Results:
- JNK inhibition disrupted leading process branching kinetics and nucleokinesis.
- Pharmacological inhibition led to centrosome and primary cilium mislocalization.
- Genetic loss of JNK impaired leading process branching and nucleokinesis, confirming JNK's intrinsic role.
Conclusions:
- JNK signaling is essential for leading process branching, nucleokinesis, and organelle trafficking during interneuron migration.
- JNK signaling plays a critical role in mediating proper cortical development.
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