FIGURE

FIGURE 9

ID

ZDB-FIG-251216-26

Publication

Chen et al., 2025 - Ddx3xa mutations drive cardiac defects in a zebrafish model via dysregulation of wnt/β-catenin signaling

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FIGURE 9

Pharmacological rescue of cardiac defects by Wnt inhibition. (A) Cardiac morphology at 72 hpf. Brightfield (A–C) and corresponding myl7:EGFP fluorescence (a'-c') views. (a,a') Wild-type (WT); (b,b') ddx3xa^−/−; myl7:EGFP homozygous mutant; (c,c') ddx3xa^−/−; myl7:EGFP mutant treated with IWR-1. Scale bar: 250 μm. (B) Heart rate quantification: ddx3xa^−/− versus IWR-1-treated ddx3xa^−/− mutants (n = 3; ***P < 0.001). (C) qRT-PCR analysis of Wnt-dependent cardiac genes (tbx5, nppb, actn2b, bmp4) in WT, WT + IWR-1, ddx3xa^−/−, and ddx3xa^−/− +IWR-1 embryos at 72 hpf (n = 3; ***P < 0.001).

Expression Data

Genes:	actn2b bmp4 nppb tbx5a
Fish:	hn1Tg (AB) ddx3xa^hn102/hn102; hn1Tg (AB)
Condition:	chemical treatment by environment: IWR-1-endo
Anatomical Term:	whole organism
Stage:	Protruding-mouth

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	ddx3xa^hn102/hn102; hn1Tg (AB)
Condition:	chemical treatment by environment: IWR-1-endo
Observed In:	atrium cardiac ventricle heart heart contraction pericardium whole organism
Stage:	Protruding-mouth

Phenotype Detail

Acknowledgments

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