Figure 2.

Eomes functional loss disrupts specification of cardiovascular progenitors.

(a) Whole-mount in situ hybridisation analysis of cardiac mesoderm (Myl7, Wnt2, Nkx2.5) and vascular (Agtrl1, Rasgrp3, Klhl6) markers in control and Eomes^N/CA;Sox2.Cre mutant embryos. Eomes mutants entirely lack expression of cardiac marker genes and show significantly reduced expression of vascular markers. In contrast in wild type embryos vascular markers broadly delineate the embryonic and extra-embryonic vasculature at E8.5-9.5. (b) Schematic diagram illustrating the protocol for generation of chimeric embryos. Eomes-null ES cells were introduced into wild type ROSA26^LacZ blastocysts. (c, d) Histological sections of two independent LacZ stained E9.5 chimeric embryos were counterstained with Eosin to identify Eomes mutant cell populations (pink). The myocardium and endocardium of the heart (he) and endoderm of the gut tube (gt) are exclusively comprised of LacZ positive wild type cells. Relatively few Eomes null cells colonize the head mesenchyme (hm), whereas the majority of other tissues are comprised of mixed populations of Eomes null and wild-type cells. Scale bar is 500 μm.