摘要：SummaryCoordinated expression of cell adhesion and signaling molecules is crucial for brain development. Here, we report that theCaenorhabditis eleganstransforming growth factor β (TGF-β) type I receptor SMA-6 (small-6) acts independently of its cognate TGF-β type II receptor DAF-4 (dauer formation-defective-4) to control neuronal guidance. SMA-6 directs neuronal development from the hypodermis through interactions with three, orphan, TGF-β ligands. Intracellular signaling downstream of SMA-6 limits expression of NLR-1, an essential Neurexin-like cell adhesion receptor, to enable neuronal guidance. Together, our data identify an atypical TGF-β-mediated regulatory mechanism to ensure correct neuronal development.Graphical abstractDisplay OmittedHighlights•TheCaenorhabditis elegansTGF-β type I receptor SMA-6 controls neuronal guidance•SMA-6 acts independently of the TGF-β type II receptor to control neuronal guidance•SMA-6 signaling limits expression of the NLR-1 neurexin-like cell adhesion receptor•Epidermal mis-expression of NLR-1 causes neuronal guidance defectsBiological sciences; Molecular neuroscience; Developmental neuroscience
