hkbis required forDIP-αexpression and target recognition in theDrosophilaneuromuscular circuit

Abstract

AbstractOur nervous system contains billions of neurons that form precise connections with each other through interactions between cell surface proteins (CSPs). InDrosophila, the Dpr and DIP immunoglobulin protein subfamilies form homophilic or heterophilic interactions to instruct synaptic connectivity, synaptic growth and cell survival. However, the upstream regulation and downstream signaling mechanisms of Dprs and DIPs are not clear. In theDrosophilalarval neuromuscular system,DIP-αis expressed in the dorsal and ventral type-Is motor neurons (MNs). We conducted an F1 dominant modifier genetic screen to identify regulators of Dprs and DIPs. We found that the transcription factor,huckebein(hkb), genetically interacts withDIP-αand is important for target recognition specifically in the dorsal Is MN, but not the ventral Is MN. Loss ofhkbled to complete removal ofDIP-αexpression. We then confirmed that this specificity is through the dorsal Is MN specific transcription factor,even-skipped(eve), which acts downstream ofhkb. Genetic interaction betweenhkbandeverevealed that they act in the same pathway to regulate dorsal Is MN connectivity. Our study provides insight into the transcriptional regulation ofDIP-αand suggests that distinct regulatory mechanisms exist for the same CSP in different neurons.