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Axonogenesis Is Coordinated by Neuron-Specific Alternative Splicing Programming and Splicing Regulator PTBP2.

Min Zhang¹, Volkan Ergin¹, Lin Lin¹

¹Division of Biomedical Sciences, University of California, Riverside, Riverside, CA 92521, USA.

|February 9, 2019

Summary

This summary is machine-generated.

The protein PTBP2 orchestrates alternative splicing in neurons, a process crucial for forming a single axon during development. This regulation ensures proper axon growth and prevents developmental defects.

Keywords:

PTB RNA binding protein SHOT1 Shootin1 axon formation nPTB neurite polarity polarization polypyrimidine-tract

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Engineering Artificial Factors to Specifically Manipulate Alternative Splicing in Human Cells

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Published on: April 26, 2017

Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

Axonogenesis, the process of forming a neuron's axon, is fundamental to neural circuit formation.
While many genes involved in axonogenesis have been identified, the coordinated regulatory mechanisms remain largely unknown.

Purpose of the Study:

To investigate the coordinated regulation of gene expression during early axon formation in primary cortical neurons.
To identify key molecular players and mechanisms governing axonogenesis.

Main Methods:

Unbiased transcriptome profiling of immature primary cortical neurons during early axon formation.
Analysis of gene expression and alternative splicing patterns.
Functional studies involving depletion or knockout of PTBP2 in vitro and in vivo.

Main Results:

Discovered a strong association between axonogenesis and neuron-specific alternative splicing, with widespread splicing changes rather than expression alterations in known axonogenesis genes.
Identified RNA-binding protein PTBP2 as a key regulator of axonogenesis-associated splicing, enriched in neurons and peaking during brain development.
Demonstrated that PTBP2 depletion leads to premature splicing changes, imbalanced isoform expression, and impaired axon formation, affecting Shtn1 splicing and actin dynamics.

Conclusions:

PTBP2-orchestrated alternative splicing programming is essential for the robust generation of a single axon in mammalian neurons.
Splicing regulation of Shtn1 by PTBP2 directly impacts actin interactions and axon growth.
Dysregulation of this splicing program, as seen in Ptbp2 knockout neurons, leads to disorganized axon formation.