BackgroundsTOR and autophagy are essential pathways to mediate anabolic and catabolic reactions, respectively, in response to various nutritional stimuli. Vertebrate development requires such reactions to achieve the common goal of generating an independent organism from a single fertilized egg.MethodsUsing the zebrafish as an animal model, we characterized the role of Wdr24, a component of the GATOR2 complex that reportedly activates TORC1.ResultsSequence analysis and subcellular localization of zebrafish Wdr24 suggested functional resemblance to its mammalian counterpart. We found that wdr24 expression commences during early embryogenesis, implicating its requirement. Accordingly, wdr24 knockdown induced defective embryogenesis accompanied by massive cell death. The developmental defects induced by wdr24 knockdown were attributable, at least in part, to dysregulated autophagy, which could be partially restored by wdr24 overexpression.ConclusionThese findings suggest that a conserved role of Wdr24 may be a critical part of the cellular metabolism in different species.