Fig. 2
- ID
- ZDB-FIG-200922-11
- Publication
- Liu et al., 2020 - CFTR deficiency causes cardiac dysplasia during zebrafish embryogenesis and is associated with dilated cardiomyopathy
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Treatment with the CFTR inhibitor CFTR_inh172 at the blastula stage leads to cardiac dysplasia in early zebrafish embryos. (A–C) The expression pattern of nkx2.5 at 13 hpf is significantly affected. Embryo orientations: dorsal view with anterior oriented at the top. Arrows indicate normal nkx2.5 expression; arrowheads demonstrate the aberrant strength and position of nkx2.5 expression in the cftr mutant; double-ended arrows indicate the distance between the two populations expressing nkx2.5. (D and E) Heart morphology (marked by the pan-cardiomyocyte marker myl7) at 24 hpf was altered significantly. Embryo orientation: ventral view with the anterior at the top. Red lines demonstrate the acute angle formed between the head midline and heart tube. (F–H) Heart morphology (marked by myl7) at 48 hpf was impaired significantly. Embryo orientation: ventral view with the anterior at the top. Arrows point to the atrium; red lines demonstrate the acute angle formed between the atrial and ventricular axes. |
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| Stage Range: | 5-9 somites to Long-pec |
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| Stage Range: | 5-9 somites to Long-pec |
Reprinted from Mechanisms of Development, 163, Liu, Y., Lin, Z., Liu, M., Liao, H., Chen, Y., Zhang, X., Chan, H.C., Zhou, B., Rao, L., Sun, H., CFTR deficiency causes cardiac dysplasia during zebrafish embryogenesis and is associated with dilated cardiomyopathy, 103627, Copyright (2020) with permission from Elsevier. Full text @ Mech. Dev.