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First published online 24 September 2003
doi: 10.1242/dev.00772
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1 Department of Genetics, Cell Biology and Development, Howard Hughes Medical
Institute, University of Minnesota, Minneapolis, MN55455, USA
2 The University of Texas at Austin, Section of Neurobiology Institute for
Cellular and Molecular Biology, 227 Patterson Laboratories, Austin, TX78712,
USA
¶ Author for correspondence (e-mail: moconnor{at}mail.med.umn.edu)
Accepted 29 July 2003
Amidated neuropeptides of the FMRFamide class regulate numerous physiological processes including synaptic efficacy at the Drosophila neuromuscular junction (NMJ). We demonstrate here that mutations in wishful thinking (wit) a gene encoding a Drosophila Bmp type 2 receptor that is required for proper neurotransmitter release at the neuromuscular junction, also eliminates expression of FMRFa in that subset of neuroendocrine cells (Tv neurons) which provide the systemic supply of FMRFa peptides. We show that Gbb, a Bmp ligand expressed in the neurohemal organ provides a retrograde signal that helps specify the peptidergic phenotype of the Tv neurons. Finally, we show that supplying FMRFa in neurosecretory cells partially rescues the wit lethal phenotype without rescuing the primary morphological or electrophysiological defects of wit mutants. We propose that Wit and Gbb globally regulate NMJ function by controlling both the growth and transmitter release properties of the synapse as well as the expression of systemic modulators of NMJ synaptic activity.
Key words: FMRFamide, Neurohemal organ, Neuromuscular junction
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