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From a screen for<jats:italic>Drosophila<\/jats:italic>mutants with aberrant synaptic development, we identified<jats:italic>beag<\/jats:italic>, a mutant with fewer synaptic boutons and decreased neurotransmitter release.<jats:italic>Beag<\/jats:italic>encodes a spliceosomal protein similar to splicing factors in humans and<jats:italic>Caenorhabditis elegans<\/jats:italic>. We find that both<jats:italic>beag<\/jats:italic>mutants and mutants of an interacting gene<jats:italic>dsmu1<\/jats:italic>have changes in the synaptic levels of specific splice isoforms of Fasciclin II (FasII), the<jats:italic>Drosophila<\/jats:italic>ortholog of neural cell adhesion molecule. We show that restoration of one splice isoform of FasII can rescue synaptic morphology in<jats:italic>beag<\/jats:italic>mutants while expression of other isoforms cannot. We further demonstrate that this FasII isoform has unique functions in synaptic development independent of transsynaptic adhesion.<jats:italic>beag<\/jats:italic>and<jats:italic>dsmu1<\/jats:italic>mutants demonstrate an essential role for these previously uncharacterized splicing factors in the regulation of synapse development and function.<\/jats:p>","DOI":"10.1523\/jneurosci.3717-11.2012","type":"journal-article","created":{"date-parts":[[2012,5,16]],"date-time":"2012-05-16T17:41:33Z","timestamp":1337190093000},"page":"7058-7073","source":"Crossref","is-referenced-by-count":34,"title":["Regulation of Fasciclin II and Synaptic Terminal Development by the Splicing Factor Beag"],"prefix":"10.1523","volume":"32","author":[{"given":"Erin S.","family":"Beck","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gabriel","family":"Gasque","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wendy 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