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Open Access Research article

Specific NuRD components are required for fin regeneration in zebrafish

Catherine Pfefferli, Fritz Müller, Anna Jaźwińska* and Chantal Wicky*

Author Affiliations

Department of Biology, University of Fribourg, Ch. du Musée 10, CH-1700 Fribourg, Switzerland

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BMC Biology 2014, 12:30  doi:10.1186/1741-7007-12-30

Published: 29 April 2014

Additional files

Additional file 1: Figure S1:

The genome of zebrafish encodes three Mi-2 orthologs. Figure S2. One of the three Mi-2 homologs, chd4a, is induced during regeneration in the adult caudal fin. Figure S3. chd4a is expressed during regenerative outgrowth in adult caudal fin. Figure S4. chd4a, chd4b, and chd3 are expressed in developing zebrafish embryos. Figure S5. The splice blocking antisense chd4a MOSP efficiently impairs the splicing of chd4a transcript. Figure S6. Zebrafish Hdac1 and human HDAC1/HDAC2 are highly conserved. Figure S7. MGCD0103 treatment does not affect the general health of zebrafish. Figure S8. Hdac1 inhibition after blastema formation is sufficient to impair regenerative outgrowth. Figure S9. The effects of MGCD0103 treatment are not reversible. Figure S10. Hdac1 inhibition and chd4a knockdown do not result in the activation of the apoptosis marker caspase-3. Figure S11. wnt5b, lef1, and msxb are expressed in chd4a morpholino oligonucleotide (MO)-injected and MGCD0103-treated fins. Figure S12. chd4a knockdown does not affect Tenascin C expression. Figure S13. chd4a knockdown reduces osteoblast proliferation. Figure S14. Hdac1 inhibition after blastema formation is sufficient to block reactivation of osteocalcin expression.

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