Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 41, Pages 14599-14604Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0507408102
Keywords
blastema; regeneration; zebrafish; genetics; stress response
Categories
Funding
- NHLBI NIH HHS [HL 02-027, T32 HL007572] Funding Source: Medline
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Zebrafish fin regeneration requires the formation and maintenance of blastema cells. Blastema cells are not derived from stem cells but behave as such, because they are slow-cycling and are thought to provide rapidly proliferating daughter cells that drive regenerative outgrowth. The molecular basis of blastema formation is not understood. Here, we show that heat-shock protein 60 (hsp60) is required for blastema formation and maintenance. We used a chemical mutagenesis screen to identify no blastema (nbI, a zebrafish mutant with an early fin regeneration defect. Fin regeneration failed in nbI due to defective blastema formation. nbI also failed to regenerate hearts. Positional cloning and mutational analyses revealed that nbI results from a V324E missense mutation in hsp60. This mutation reduced hsp60 function in binding and refolding denatured proteins. hsp60 expression is increased during formation of blastema cells, and dysfunction leads to mitochondrial defects and apoptosis in these cells. These data indicate that hsp60 is required for the formation and maintenance of regenerating tissue.
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