Fig. S4
- ID
- ZDB-FIG-161110-18
- Publication
- Cheng et al., 2016 - Vinculin b deficiency causes epicardial hyperplasia and coronary vessel disorganization in zebrafish
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Cardiac progenitor specification and early ventricular development are relatively normal in v12 mutants. (A-D) vclb mRNA is greatly reduced in the mutants at 30 hpf revealed by whole mount in situ hybridization(B), particular in the heart at 48 hpf (D) compared with wildtype siblings (A, C).Arrow points to the heart (C). (E-H) Cardiac progenitor markers cmlc2 and nkx2.5 are not affected in v12 mutants(F, H) compared with wildtype siblings (E, G) at early heart-tube formation stages. (I-P) Ventricular markers vmhc and nppa are not affected in v12 mutants (J, N, L, P) compared with wildtype siblings (I, K, M, O) from 36 to 84 hpf. |