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Alternative RNA Splicing02:18

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Control of neuronal synapse specification by a highly dedicated alternative splicing program.

Lisa Traunmüller1, Andrea M Gomez1, Thi-Minh Nguyen1

  • 1Biozentrum, University of Basel Klingelbergstrasse 50-70, 4056 Basel, Switzerland.

Science (New York, N.Y.)
|May 14, 2016
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Summary
This summary is machine-generated.

The RNA-binding protein SLM2 controls specific gene splicing in the mouse hippocampus, impacting synaptic function. Correcting a single gene target in SLM2 knockout mice restored normal synaptic plasticity and behavior.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Alternative RNA splicing allows genomes to increase coding capacity.
  • RNA-binding proteins regulate alternative splicing, influencing protein function and quantity.
  • Glutamatergic synapses are crucial for learning and memory in the central nervous system.

Purpose of the Study:

  • To investigate the role of the RNA-binding protein SLM2 in synaptic function.
  • To identify SLM2-regulated alternative splicing targets in the mouse hippocampus.
  • To determine if SLM2-dependent splicing is essential for synaptic plasticity and behavior.

Main Methods:

  • Genome-wide mapping of SLM2-dependent alternative splicing events.
  • Genetic manipulation of SLM2 in mouse models.
  • Assessment of synaptic plasticity and behavioral assays in Slm2 knockout mice.
  • Targeted genetic correction of a specific SLM2-dependent exon in neurexin-1.

Main Results:

  • SLM2 regulates a highly selective splicing program of synaptic protein-encoding messenger RNAs.
  • SLM2 is essential for the functional specification of glutamatergic synapses in the hippocampus.
  • Genetic correction of a single SLM2 target exon in neurexin-1 rescued synaptic plasticity and behavioral deficits in Slm2 knockout mice.

Conclusions:

  • SLM2 controls a specific alternative splicing program critical for synaptic properties.
  • This selective splicing program is vital for central nervous system function.
  • Targeting SLM2-dependent splicing offers a potential avenue for understanding and treating neurological disorders.