During organ development, controlled differentiation makes the right constituent cell types, while tissue morphogenesis creates the right 3D structure to support function. How are these two seemingly independent processes coordinated? In the zebrafish olfactory epithelium, two waves of neurogenesis create olfactory neurons in a manner requiring the transcription factors Neurog1 and Neurod4; concomitantly, olfactory progenitors are shaped into a cup by coordinated cell migration in a process controlled by the chemokine receptor Cxcr4b and its ligand Cxcl12a. Now, Raphaël Aguillon and colleagues reveal that Neurog1 acts on Cxcr4b to control olfactory morphogenesis. In neurog1 mutant zebrafish embryos, oriented cell movements of early-born olfactory neurons (EON), specifically in the anterior region, fail to occur normally, even though EON mobility itself is not affected. Similar defects are observed in cxcr4b and cxcl12a mutants. In neurog1 mutants, cxcr4b (but not cxcl12a) expression is lost early in EON progenitors, before it recovers later on. Restoring early expression of cxcr4b in neurog1 mutants rescues the migration phenotype. Finally, the authors identify a CAGATG E-box cluster upstream of cxcr4b that is directly regulated by Neurog1. Thus, Neurog1 provides a bridge between neurogenesis and morphogenesis.
