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Regulation of Fasciclin II and Synaptic Terminal Development by the Splicing Factor Beag

Authors :
Gabriel Gasque
Wei Wei Jiao
Pao Shu Wu
Ben Jiwon Choi
Wendy L. Imlach
Erin S. Beck
Brian D. McCabe
Matthew L. Kraushar
Source :
The Journal of Neuroscience. 32:7058-7073
Publication Year :
2012
Publisher :
Society for Neuroscience, 2012.

Abstract

Pre-mRNA alternative splicing is an important mechanism for the generation of synaptic protein diversity, but few factors governing this process have been identified. From a screen forDrosophilamutants with aberrant synaptic development, we identifiedbeag, a mutant with fewer synaptic boutons and decreased neurotransmitter release.Beagencodes a spliceosomal protein similar to splicing factors in humans andCaenorhabditis elegans. We find that bothbeagmutants and mutants of an interacting genedsmu1have changes in the synaptic levels of specific splice isoforms of Fasciclin II (FasII), theDrosophilaortholog of neural cell adhesion molecule. We show that restoration of one splice isoform of FasII can rescue synaptic morphology inbeagmutants while expression of other isoforms cannot. We further demonstrate that this FasII isoform has unique functions in synaptic development independent of transsynaptic adhesion.beaganddsmu1mutants demonstrate an essential role for these previously uncharacterized splicing factors in the regulation of synapse development and function.

Details

ISSN :
15292401 and 02706474
Volume :
32
Database :
OpenAIRE
Journal :
The Journal of Neuroscience
Accession number :
edsair.doi.dedup.....1606fc0a335d67c21028912d9a6bf454
Full Text :
https://doi.org/10.1523/jneurosci.3717-11.2012