<i>fgf20</i> Is Essential for Initiating Zebrafish Fin Regeneration

  • Geoffrey G. Whitehead
    Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.
  • Shinji Makino
    Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.
  • Ching-Ling Lien
    Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.
  • Mark T. Keating
    Howard Hughes Medical Institute, Department of Cell Biology, Harvard Medical School, Department of Cardiology, Children's Hospital, Boston, MA 02115, USA.

抄録

<jats:p> Epimorphic regeneration requires the presence or creation of pluripotent cells capable of reproducing lost organs. Zebrafish fin regeneration is mediated by the creation of blastema cells. Here, we characterize the <jats:italic>devoid of blastema</jats:italic> ( <jats:italic>dob</jats:italic> ) mutant that fails fin regeneration during initial steps, forms abnormal regeneration epithelium, and does not form blastema. This mutation has no impact on embryonic survival. <jats:italic>Dob</jats:italic> results from an <jats:italic>fgf20a</jats:italic> null mutation, Y148S. <jats:italic>Fgf20a</jats:italic> is expressed during initiation of fin regeneration at the epithelial-mesenchymal boundary and later overlaps with the blastema marker <jats:italic>msxb</jats:italic> . Thus, <jats:italic>fgf20a</jats:italic> has a regeneration-specific requirement, initiating fin regeneration, and controlling blastema formation. </jats:p>

収録刊行物

  • Science

    Science 310 (5756), 1957-1960, 2005-12-23

    American Association for the Advancement of Science (AAAS)

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