Nodal-dependent mesendoderm specification requires the combinatorial activities of FoxH1 and Eomesodermin.

ABSTRACT: Vertebrate mesendoderm specification requires the Nodal signaling pathway and its transcriptional effector FoxH1. However, loss of FoxH1 in several species does not reliably cause the full range of loss-of-Nodal phenotypes, indicating that Nodal signals through additional transcription factors during early development. We investigated the FoxH1-dependent and -independent roles of Nodal signaling during mesendoderm patterning using a novel recessive zebrafish FoxH1 mutation called midway, which produces a C-terminally truncated FoxH1 protein lacking the Smad-interaction domain but retaining DNA-binding capability. Using a combination of gel shift assays, Nodal overexpression experiments, and genetic epistasis analyses, we demonstrate that midway more accurately represents a complete loss of

SUBMITTER: Slagle CE 

PROVIDER: S-EPMC3102743 | biostudies-literature | 2011 May

REPOSITORIES: biostudies-literature