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RBM4 Modulates Radial Migration via Alternative Splicing of Dab1 during Cortex Development
Dhananjaya D1,2, Kuan-Yang Hung2, Woan-Yuh Tarn3,2
1Taiwan International Graduate Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, Taiwan.
Molecular and Cellular Biology
|March 28, 2018
Summary
RNA-binding motif 4 (RBM4) protein is crucial for embryonic brain development, regulating neuronal migration by controlling Disabled-1 (Dab1) splicing. Its absence causes developmental brain abnormalities.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- RNA-binding motif 4 (RBM4) regulates mRNA splicing for tissue-specific gene expression.
- RBM4 is expressed in the developing embryonic brain, particularly in neuronal progenitor zones.
- Dysregulation of neuronal migration is linked to developmental brain abnormalities.
Purpose of the Study:
- To investigate the role of RBM4 in embryonic brain development and neuronal migration.
- To identify downstream targets of RBM4 involved in these processes.
- To elucidate the mechanism by which RBM4 influences neuronal migration.
Main Methods:
- Utilized Rbm4a knockout mouse models and in utero electroporation for RBM4 knockdown.
- Performed RNA immunoprecipitation followed by high-throughput sequencing (RIP-Seq) to identify RBM4 targets.
- Analyzed Disabled-1 (Dab1) splicing patterns and performed rescue experiments.
Main Results:
- Rbm4a knockout brains showed delayed neuronal migration.
- RBM4 knockdown impaired cortical neuronal migration.
- Disabled-1 (Dab1) was identified as a direct RBM4 target, with RBM4 promoting inclusion of Dab1 exons 7 and 8.
- Full-length Dab1 expression rescued RBM4-depletion-induced migration defects.
Conclusions:
- RBM4 is essential for proper neuronal migration during embryonic brain development.
- RBM4 regulates neuronal migration by modulating the alternative splicing of Dab1.
- RBM4 deficiency can lead to developmental brain abnormalities due to impaired neuronal migration.
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