Fig. 4

Fig. 4 Loss of Mef2c function abolishes sarcomeric gene expression. Hearts of 48–50 hpf (A–F) or 72 hpf (G) mef2ca^b1086;mef2cb^fh288 mutant embryos and their siblings in bright field (A), after immunodetection (C,D and G) or in situ mRNA hybridisation (B,E and F) shown in lateral view, anterior to left (A and G) or ventral (B–F) view, anterior to top. A.mef2ca^b1086;mef2cb^fh288 embryos had a tiny residual heart (arrow) and cardiac chamber edema. B,E and F. Double mutant embryos lacked almost all myl7, vmhc, bmp4 and nppa mRNAs as well as MyHC and Mef2 proteins in ventricle (v), atrium (a) or AV canal (red arrows in F) except for one (arrows in C,E) or two small heart structures expressing these markers. C. Confocal stack showing genotyped double mutant expressing low levels MyHC and nuclear Mef2 in a residual myocardial tissue. Sibling presented is mef2ca^+/b1086;mef2cb^+/+. D. No MyHC or atrial MyHC is detected in mef2d/c morphants. G. Immunodetection for GFP (atrium and ventricle, green) and Elastin (bulbus arteriosus, ba) in hearts of three different genotyped mef2ca^b1086;mef2cb^fh288;Tg(myl7:EGFP)twu26 showing variation in residual differentiated myocardial and bulbus tissue, compared to the normal heart of a mef2ca^+/b1086;mef2cb^+/fh288;Tg(myl7:EGFP)twu26 sibling. Scale=100 μm. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)