Fig. S6
Mef2ca and Mef2cb dual loss of function abolishes myocardial differentiation.
A,B. In situ mRNA hybridisation for myl7 in hearts of 24 hpf mef2cab1086;mef2cbfh288 mutant embryos and their siblings (A) or control and mef2cb+/fh288 incross embryos non-injected or injected with mef2ca MO, shown in a dorsal view, anterior to top. Double mutants have almost no myl7 expression albeit few cells in the cardiac region (arrows, A). Mef2cbfh288 mutant embryos injected with mef2ca MO have a thinner than normal heart tube. All other control or embryos with only one Mef2 depleted have a normal heart. C. Bright field images of mef2cbfh288 mutant embryos injected with mef2ca MO showing cardiac edema, compared with mef2ca MO injected siblings with normal heart and no edema. Scale = 100 μm.
Reprinted from Developmental Biology, 369(2), Hinits, Y., Pan, L., Walker, C., Dowd, J., Moens, C.B., and Hughes, S.M., Zebrafish Mef2ca and Mef2cb are essential for both first and second heart field cardiomyocyte differentiation, 199-210, Copyright (2012) with permission from Elsevier. Full text @ Dev. Biol.