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Fig. 7 Suppression of RA levels expands cardiac myosin expressing-cells (cmlc2) in cdx-deficient embryos, and can be rescued by exogenous RA treatment. Expression of cmlc2 expression in wildtype, cdx4 and cdx1a/4-deficient embryos incubated with DMSO (control), DEAB, or DEAB and RA, was assayed by whole mount in situ hybridization at the 16 somite stage. cdx mutants evinced dramatic expansion of cardiac mesoderm when RA production was abrogated, and this phenotype was rescued by concomitant DEAB and RA treatment.
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Reprinted from Developmental Biology, 354(1), Lengerke, C., Wingert, R., Beeretz, M., Grauer, M., Schmidt, A.G., Konantz, M., Daley, G.Q., and Davidson, A.J., Interactions between Cdx genes and retinoic acid modulate early cardiogenesis, 134-142, Copyright (2011) with permission from Elsevier. Full text @ Dev. Biol.