CONVERSION OF ZEBRAFISH BLASTOMERES TO AN ENDODERMAL FATE BY TGF-BETA-RELATED SIGNALING

The endoderm contributes cells to the gut, and participates in the ind uction and patterning of the vertebrate head and heart. The mechanisms controlling the formation of endoderm are poorly understood. Commitme nt of endoderm cells occurs at the onset of gastrulation and requires cell interactions [1]; studies in vitro have implicated transforming g rowth factor beta (TGF-beta)-related molecules in this process [2,3], TARAM-A is a zebrafish receptor kinase that is related to the type I s ubunit of the TGF-P receptor, and is expressed in presumptive endomeso dermal cells at gastrulation [4], We provide here evidence for its inv olvement in endoderm formation in vivo. Activation of TARAM-A was foun d to drive blastomeres towards an endodermal fate. The induced endoder m behaved as endogenous endoderm during gastrulation: it migrated in c ontact with the yolk and expressed endoderm-specific markers. Loss of- function mutations in the zebrafish one-eyed-pinhead (oep) gene lead t o defects in heart formation, defects of the ventral central nervous s ystem (CMS) and cyclopia [5-7]. Mutant embryos also lack endoderm and anterior mesoderm. Endoderm formation in oep mutant embryos was found to be restored by the activation of the TARAM-A signalling pathway. Ca rdiac and ocular defects, but not midline CNS structures, were rescued non-autonomously, demonstrating that endoderm may provide signals tha t can pattern the eye anlage, and which ape distinct from those specif ying the ventral midline of the CNS. (C) Current Biology Ltd.