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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.