Fig. 6
- ID
- ZDB-FIG-250725-25
- Publication
- Deng et al., 2025 - Gremlin1 repression-mediated mitochondrial network hyperfunction contributes to TCE-induced zebrafish cardiac defects
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Gene features combined with myocardial ultrastructure reveal the aberrant mitochondria function in grem1a-knockdown cardiomyocytes of zebrafish. A–B Pseudo-time trajectory analysis of the myocardial clusters 1–3. C BEAM analysis of cardiomyocyte genes based on their expression patterns across the branchpoint. GO analysis of genes in D cluster 1 and E cluster 3. F The ultrastructure of (a–a`) cardiomyocytes in zebrafish at 72 hpf and (b–b`) corresponding magnification images of mitochondria (n = 7). In grem1a-KD zebrafish, some longitudinal myofibrils (yellow arrows) were interrupted by vacuole. The boundary of bright band (black arrows) and dark band (red arrows) were not clear. Mitochondria (circled by yellow dashed lines) in grem1a-KD zebrafish were increased in the size and number with denser cristae |