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PQBP1 regulates striatum development through balancing striatal progenitor proliferation and differentiation
Wenhua Liu1, Hao Xie1, Xian Liu1
1School of Life Science and Technology, the Key Laboratory of Developmental Genes and Human Disease, Southeast University, 2 Sipailou Road, Nanjing 210096, China.
Cell Reports
|March 21, 2023
Summary
The alternative splicing regulator PQBP1 is crucial for brain development. Its absence impairs neurogenesis by reducing progenitor proliferation, offering insights into Renpenning syndrome.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- Maintaining the balance between neural progenitor cell proliferation and differentiation is vital for brain development.
- While transcriptional regulation is well-studied, post-transcriptional mechanisms controlling these processes are less understood.
Purpose of the Study:
- To investigate the role of the alternative splicing regulator PQBP1 in striatal progenitor cell proliferation and differentiation.
- To elucidate the molecular mechanisms by which PQBP1 influences neurogenesis and brain development.
Main Methods:
- Utilizing genetic deletion of PQBP1 in striatal progenitors.
- Analyzing cell proliferation and differentiation markers.
- Investigating PQBP1 interactions with splicing machinery.
- Performing alternative splicing profiling.
Main Results:
- Deletion of PQBP1 in striatal progenitors leads to defective striatal development and impaired neurogenesis of spiny projection neurons (SPNs).
- PQBP1-deficient progenitors show decreased proliferation and increased differentiation, shrinking the progenitor pool.
- PQBP1 interacts with splicing machinery components.
- PQBP1 promotes the inclusion of exon 9 in Numb mRNA, a variant linked to progenitor proliferation.
Conclusions:
- PQBP1 acts as a key regulator in balancing striatal progenitor proliferation and differentiation.
- PQBP1's function in Numb splicing is critical for maintaining the neural progenitor pool.
- Dysregulation of PQBP1 may contribute to the pathogenesis of Renpenning syndrome.
