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Development 135 (18): 3063-3070

Fgfs control homeostatic regeneration in adult zebrafish fins

Airon A. Wills*, Ambrose R. Kidd, III*, Alexandra Lepilina, and Kenneth D. Poss{dagger}

Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.

{dagger} Author for correspondence (e-mail: k.poss{at}cellbio.duke.edu)

Accepted for publication 16 July 2008.

Abstract: Adult teleost fish and urodele amphibians possess a spectacular ability to regenerate amputated appendages, based on formation and maintenance of progenitor tissue called a blastema. Although injury-induced, or facultative, appendage regeneration has been studied extensively, the extent to which homeostatic regeneration maintains these structures has not been examined. Here, we found that transgenic inhibition of Fgf receptors in uninjured zebrafish caused severe atrophy of all fin types within 2 months, revealing a requirement for Fgfs to preserve dermal bone, joint structures and supporting tissues. Appendage maintenance involved low-level expression of markers of blastema-based regeneration, focused in distal structures displaying recurrent cell death and proliferation. Conditional mutations in the ligand Fgf20a and the kinase Mps1, factors crucial for regeneration of amputated fins, also caused rapid, progressive loss of fin structures in otherwise uninjured animals. Our experiments reveal that the facultative machinery that regenerates amputated teleost fins also has a surprisingly vigorous role in homeostatic regeneration.

Key Words: Blastema • Fgf • Fin • Homeostasis • Regeneration • Zebrafish


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