Fig. 1. Loss of Hdac1/Hdac2 within Nkx2.5^IRES-Cre+ cells causes defective cardiogenesis and complete embryonic lethality.

(A) Nkx2.5^IRES-Cre;1^F+2^F+ was crossed with 1^FF2^FF, and samples were recovered at various time points. ^aThree embryos dying. *P < 0.05; ns, not significant. (B) Nkx2.5;1^KO2^KO and 1^FF2^FF embryos at embryonic day 11.5 (E11.5) (arrows, pooled blood). (C) Nkx2.5;1^Het2^Het;R26R-LacZ^−/+ and Nkx2.5;1^KO2^KO;R26R-LacZ^−/+ E10.5 embryos. (D) Hematoxylin and eosin–stained Nkx2.5;1^Het2^Het and Nkx2.5;1^KO2^KO E10.5 sagittal sections at atrioventricular canal (AVC) level (arrows, eosinophilic cytoplasm; bars, compact thickness). (E) Compact myocardial thickness in control and Nkx2.5;1^KO2^KO E10.5 primitive ventricles (PrVs). (F) Transmission electron micrographs (TEMs) of Nkx2.5;1^KO2^KO and 1^FF2^FF E10.5 cardiomyocytes (blue, contractile fibers; orange, cytoplasmic lipid droplets). (G) TEM of Nkx2.5;1^KO2^KO and 1^FF2^FF E10.5 cardiomyocyte mitochondrial structure, density, and size.