Heat-shock protein 60 is required for blastema formation and maintenance during regeneration
AUTOR(ES)
Makino, Shinji
FONTE
National Academy of Sciences
RESUMO
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 (nbl), a zebrafish mutant with an early fin regeneration defect. Fin regeneration failed in nbl due to defective blastema formation. nbl also failed to regenerate hearts. Positional cloning and mutational analyses revealed that nbl 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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1253607Documentos Relacionados
- Evidence for protection by heat-shock proteins against photoinhibition during heat-shock
- Heat-shock protein 104 expression is sufficient for thermotolerance in yeast.
- Archaebacterial heat-shock proteins
- lon gene product of Escherichia coli is a heat-shock protein.
- Heat-shock protein hsp90 governs the activity of pp60v-src kinase.