Microtubules function in TGF-β signalling by facilitating the cytoplasmic trafficking of internalized receptors and the nucleocytoplasmic shuttling of Smads. However, nothing is known about whether actin filaments are required for these processes. Here we report that zebrafish actin-bundling protein fscn1a is highly expressed in mesendodermal precursors and its expression is directly regulated by the TGF-β superfamily member Nodal. Knockdown or knockout of fscn1a leads to a reduction of Nodal signal transduction and endoderm formation in zebrafish embryos. Fscn1 specifically interacts with TGF-β family type I receptors, and its depletion disrupts the association between receptors and actin filaments and sequesters the internalized receptors into clathrin-coated vesicles. Therefore, Fscn1 acts as a molecular linker between TGF-β family type I receptors and the actin filaments to promote the trafficking of internalized receptors from clathrin-coated vesicles to early endosomes during zebrafish endoderm formation.

As one of the largest internal organs in the body, liver is very important for metabolism, detoxification and homeostasis. It's reported that liver development is accurately regulated by a gene regulating network consists of FGF, BMP, WNT signal pathways and a lot of transcription factors. However, the functions of microRNA are poorly understood during liver formation. In recent years, it has been reported that mir122 is highly expressed in hepatocytes, and plays a vital role in the metabolic processes of the liver, but its function in liver development remains unclear. In this study, we report that mir122 is specifically expressed in zebrafish (Danio rerio) embryonic liver, and its expression level is notably increased during the differentiation process of hepatoblast into hepatocyte. mir122 inactivation by an antisense morpholino has no influence on the specification, budding and outgrowth of hepatoblast. However, zbrafish hepatoblast can not differentiate into hepatocyte without mir122. Therefore, mir122 is not only involved in liver metabolic functions, but also indispensable for hepatoblast differentiation.