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. 2008 Feb 19;105(8):2913–2918. doi: 10.1073/pnas.0712344105

Fig. 4.

Fig. 4.

Transgenic reporter lines reveal OFT defects and normal FHF contribution in Raldh2−/− embryos. (A and B) Right-side views of X-gal stained E9 WT and Raldh2−/− embryos, showing absence of y96-Myf5-nlacZ-16 transgene expression, a marker of the OFT (arrowheads), in the mutant. (C and D) In Mlc3f-nlacZ-9 hearts at the 14-somite stage, X-gal staining distinguishes the OFT lacking transgene activity (C, bracket) and the right ventricle. β-Gal activity is also detected in the left ventricle. The nonexpressing domain (presumptive OFT) is absent under RA deficiency (D). The white lines indicate planes of sections in C′ and D′. (E and F) At the eight-somite stage, Mlc3f-nlacZ-2E transgene expression marks the presumptive right atria and left ventricle in both WT (E) and Raldh2−/− mutants (F). (G and H) Ventral views of X-gal stained Mlc3f-nlacZ-2E WT and Raldh2−/− embryos at the 16-somite stage showing the distinction between right (arrowheads) and left ventricles. White lines indicate planes of sections in G′ and H′. ra, right atria.

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