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. 2009 Jan 7;106(3):814–819. doi: 10.1073/pnas.0807583106

Fig. 3.

Fig. 3.

Etsrp71 is essential for cardiac morphogenesis and specification of the endocardial/endothelial lineage. (A) Schematic of the Etsrp71 gene and the targeted disruption. (B) (Top) Morphological appearance of E8.5 +/+ and Etsrp71 −/− embryo littermates. Note that the whole-mount WT and Etsrp71 mutant embryos are indistinguishable at E8.5. (Middle) Histological analyses of the WT and null embryo demonstrating an absence of the endocardial/endothelial lineage (End) and vasculature (PHV, primary heart vein; DA, dorsal aorta) in the null embryo compared to WT littermate. (Bottom) Immunohistochemical analysis of α-endomucin in the WT and Etsrp71 null embryo further demonstrating an absence of the endocardial/endothelial lineage (arrowhead shown in WT) and an absence of the vasculature in the null embryo. A higher magnification field reveals an absence of endocardium in the null heart compared to the WT littermate (α-endomucin expressing endocardium indicated by an arrowhead). (C) qRT-PCR analyses using purified RNA from individual Etsrp71 WT (black) and null (white) E8.5 hearts (performed in triplicate). Transcript level in the WT heart was considered to be 1 and Etsrp71 transcript was not detectable in the mutant heart (*). Note the significant downregulation of Flk1 transcripts and the essential absence of Tie2 transcripts in the Etsrp71 mutant heart (**, P < 0.001). Each assay was analyzed in triplicate and repeated twice.