Regulation of central neuron synaptic targeting by the Drosophila POU protein, Acj6

Mutations in the Drosophila class IV POU domain gene, abnormal chemosensory jump d (acj6), have previously been shown to cause physiological deficits in odor sensitivity, However, loss of Acj6 function also has a severe detri mental effect upon coordinated larval and adult movement that cannot be exp lained by the simple loss in odorant detection. Tn addition to olfactory se nsory neurons, Acj6 is expressed in a distinct subset of postmitotic intern eurons in the central nervous system from late embryonic to adult stages. I n the larval and adult brain, Acj6 is highly expressed in central brain, op tic and antennal lobe neurons. Loss of Acj6 function in larval optic lobe n eurons results in disorganized retinal axon targeting and synapse selection . Furthermore, the lamina neurons themselves exhibit disorganized synaptic arbors in the medulla of acj6 mutant pupal brains, suggesting that Acj6 may play a role in regulating synaptic connections or structure. To further te st this hypothesis, we misexpressed two Acj6 isoforms in motor neurons wher e they are not normally found, The two Acj6 isoforms are produced from alte rnatively spliced acj6 transcripts, resulting in significant structural dif ferences in the amino-terminal POU IV box. Acj6 misexpression caused marked alterations at the neuromuscular junction, with contrasting effects upon n erve terminal branching and synapse formation associated with specific Acj6 isoforms, Our results suggest that the class IV POU domain factor, Acj6, m ay play an important role in regulating synaptic target selection by centra l neurons and that the amino-terminal POU IV box is important for regulatio n of Acj6 activity.