Molecular Mechanisms of Cortex Glial Morphology in Drosophila

Glia have emerged as important components of numerous nervous system functions. While there has been significant research devoted to glial interactions with the axon and synapse, many glial subtypes form contacts with the neuronal cell body, and their roles are not well understood. Cortex glia, a Drosophila glial subtype, provide an excellent model for investigating glia-neuronal cell body interactions. Previous research has implicated soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein α (αSNAP) as a necessary regulator of cortex glial morphology, and its expression in cortex glia is important for normal calcium signaling and normal cortex glial infiltration. Additionally, cortex glia that lack αSNAP fail to proliferate. Here, by interrupting mitotic divisions and cell proliferation in cortex glia, we show that cortex glial proliferation is not responsible for defective infiltration in αSNAP knockdowns. Previous work has also found that αSNAP mediates the exocytosis of Spätzle 3 (Spz3) in cortex glia, a secreted neurotrophin required to maintain cortex glial morphology; however, the precise downstream mechanisms are unclear. In this study, we identify potential downstream signaling interactors of Spz3. In particular, we focus on a potential Spz3 binding partner, secreted Wingless-interacting molecule (Swim), to understand the mechanisms underlying cortex glial morphology in vivo