Dusp1 modulates activin/smad2 mediated germ layer specification via FGF signal inhibition in embryos.

Activin, a member of the transforming growth factor (TGF-β) superfamily, induces mesoderm, endoderm and neuro-ectoderm formation in embryos. Despite several previous studies, the complicated gene regulatory network and genes involved in this induction await more elaboration. We identified expression of various fibroblast growth factor (FGF) genes in activin/ treated animal cap explants (AC) of embryos. Activin/ increased / expression, which was reduced by co-injection of dominant negative activin receptor (DNAR) and dominant negative Fgf receptor (DNFR). Interestingly, activin/ also increased expression of () which has been known to inhibit Fgf signaling. overexpression in dorsal marginal zone caused gastrulation defect and decreased Jnk/Erk phosphorylation as well as Smad1 linker region phosphorylation. decreased neural and organizer gene expression with increasing of endodermal and ventral gene expression in treated AC, indicating that modulates germ layer specification. decreased neural gene expression in treated AC, suggesting that Erk and/or Jnk phosphorylation may be involved in induced neural induction. In addition, decreased the reporter gene activities of activin response element (ARE) and increased it for bmp response element (BRE), indicating that modulates two opposite morphogen signaling of dorsal (activin/Smad2) and ventral (bmp/Smad1) tracks, acting to fine tune the Fgf/Erk pathway.