Fig. S10
- ID
- ZDB-FIG-110915-33
- Publication
- Totong et al., 2011 - The novel transmembrane protein Tmem2 is essential for coordination of myocardial and endocardial morphogenesis
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Myocardial expression of tmem2 rescues myocardial and endocardial fusion defects in MZfrv mutants. (A-D) Dorsal views depict myl7 expression at 24 hpf. (E-H) Dorsal views depict endocardial expression of cdh5 (arrowheads) at 24 hpf. (A,B,E,F) Expression of Tg(myl7:tmem2-gfp) has no effects on myocardial or endocardial morphogenesis in Mfrv embryos. (C,D) Expression of Tg(myl7:tmem2-gfp) rescues myocardial fusion in MZfrv embryos. The rate of cardiomyocyte movement varies among MZfrv mutants, such that some mutants exhibit contact between contralateral populations of cardiomyocytes at 24 hpf (C), whereas others do not exhibit any contact even at 26 hpf (see Fig. 4I). Even so, expression of Tg(myl7:tmem2-gfp) always results in significant acceleration of myocardial morphogenesis in MZfrv mutants. In this example (D), myocardial fusion is complete and myocardial tube extension has initiated. (G,H) Expression of Tg(myl7:tmem2-gfp) rescues endocardial fusion in MZfrv embryos. In this example (H), endocardial fusion is complete and endocardial tube extension has begun. Non-transgenic (non-tg) and transgenic siblings were distinguished by examination of fluorescence before fixation. Comparable results were obtained with two independent transgenic founders. Scale bar: 50 μm. |