The T-box transcription factor Eomesodermin acts upstream of Mesp1 to specify cardiac mesoderm durin

Author:  ["Ita Costello","Inga-Marie Pimeisl","Sarah Dräger","Elizabeth K. Bikoff","Elizabeth J. Robertson","Sebastian J. Arnold"]

Publication:  Nature Cell Biology

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Tags:  Gastrulation   Biological

Abstract

T-box transcription factor Eomes acts during gastrulation to promote mesoderm migration and specification of the definitive endoderm. Robertson and colleagues report a further role for Eomes in directing the specification of the cardiac lineage through activation of Mesp1 upstream of the cardiac transcriptional machinery at the gastrulation stage. Instructive programmes guiding cell-fate decisions in the developing mouse embryo are controlled by a few so-termed master regulators. Genetic studies demonstrate that the T-box transcription factor Eomesodermin (Eomes) is essential for epithelial-to-mesenchymal transition, mesoderm migration and specification of definitive endoderm during gastrulation1. Here we report that Eomes expression within the primitive streak marks the earliest cardiac mesoderm and promotes formation of cardiovascular progenitors by directly activating the bHLH (basic-helix-loop-helix) transcription factor gene Mesp1 upstream of the core cardiac transcriptional machinery2,3,4. In marked contrast to Eomes/Nodal signalling interactions that cooperatively regulate anterior–posterior axis patterning and allocation of the definitive endoderm cell lineage1,5,6,7,8, formation of cardiac progenitors requires only low levels of Nodal activity accomplished through a Foxh1/Smad4-independent mechanism. Collectively, our experiments demonstrate that Eomes governs discrete context-dependent transcriptional programmes that sequentially specify cardiac and definitive endoderm progenitors during gastrulation.

Cite this article

Costello, I., Pimeisl, IM., Dräger, S. et al. The T-box transcription factor Eomesodermin acts upstream of Mesp1 to specify cardiac mesoderm during mouse gastrulation. Nat Cell Biol 13, 1084–1091 (2011). https://doi.org/10.1038/ncb2304

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