Abstract
The insulin-producing cells (IPCs), a group of 14 neurons in the Drosophila brain, regulate numerous processes, including energy homeostasis, lifespan, stress response, fecundity, and various behaviors, such as foraging and sleep. Despite their importance, little is known about the development and the factors that regulate morphological and functional differentiation of IPCs. In this study, we describe the use of a new transgenic reporter to characterize the role of the Drosophila L1-CAM homolog Neuroglian (Nrg), and the transmembrane Semaphorin-1a (Sema-1a) and its receptor Plexin A (PlexA) in the differentiation of the insulin-producing neurons. Loss of Nrg results in defasciculation and abnormal neurite branching, including ectopic neurites in the IPC neurons. Cell-type specific RNAi knockdown experiments reveal that Nrg, Sema-1a and PlexA are required in IPCs and glia to control normal morphological differentiation of IPCs albeit with a stronger contribution of Nrg and Sema-1a in glia and of PlexA in the IPCs. These observations provide new insights into the development of the IPC neurons and identify a novel role for Sema-1a in glia. In addition, we show that Nrg, Sema-1a and PlexA in glia and IPCs not only regulate morphological but also functional differentiation of the IPCs and that the functional deficits are likely independent of the morphological phenotypes. The requirements of nrg, Sema-1a, and PlexA in IPC development and the expression of their vertebrate counterparts in the hypothalamic-pituitary axis, suggest that these functions may be evolutionarily conserved in the establishment of vertebrate endocrine systems.
Highlights
The insulin-producing cells (IPCs) are a cluster of 14 neurosecretory neurons located in the pars intercerebralis of the Drosophila brain
To investigate whether nrg is required for normal IPC development, we generated an IPC marker in which the expression of the somatodendritic marker DenMark is under the direct control of the dilp2 promoter [1, 40]
We identify the requirement of three genes, nrg, Sema-1a, and Plexin A (PlexA) in the morphological and functional differentiation of IPC neurons, and identify glia as a source of morphoregulators controlling neuritogenesis of the IPCs
Summary
The insulin-producing cells (IPCs) are a cluster of 14 neurosecretory neurons located in the pars intercerebralis of the Drosophila brain. The IPCs are the major source of the Drosophila insulin-like peptides (Dilps). They express Dilp2, -3, and -5, which are secreted into the circulatory hemolymph via contacts on the aorta [1]. It was later shown that the transcription factor Dachshund regulates dilp transcription via an interaction with Eyeless, but no defects in IPC differentiation were reported in dachshund loss-of-function animals [7]. A study to identify factors contributing to insulin-like peptide production identified a role for Unc-104 and Rab in IPC development, where loss of either protein resulted in larvae with reduced IPC cell number and aberrant IPC morphology [8]
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