Fig. 6
- ID
- ZDB-IMAGE-140902-27
- Genes
- Antibodies
- Publication
- Pfefferli et al., 2014 - Specific NuRD components are required for fin regeneration in zebrafish
- All Figures
- Figures for Pfefferli et al., 2014
Fig. 6
Hdac1 inhibition and morpholino-mediated knockdown of chd4a, mta2, and the two rbb4 orthologs cause abnormal expression of Actinodin 1. (A-B) Longitudinal sections of fin regenerates at 4 dpa treated with DMSO (A) or MGCD0103 (B) and stained with Tenascin C antibody (red) and DAPI (blue). Mesenchymal remodeling was not altered in MGCD0103-treated fins. (C-H) Longitudinal sections of fin regenerates at 4 dpa treated with DMSO (C) or MGCD0103 (D), or injected with control (E), chd4a (F), mta2 (G), or rbb4 + rbb4l (H) MOs stained with Actinodin 1 antibody (green) and DAPI (blue). Depletion of the NuRD components hdac1, chd4a, mta2, or rbb4/rbb4l resulted in a disorganized expression pattern of Actinodin 1. Dashed lines indicate the amputation plane. Scale bars: 100 μm.