Mar 4, 2020

A metabolic shift to glycolysis promotes zebrafish tail regeneration through TGF-β dependent dedifferentiation of notochord cells to form the blastema

Jason W. SinclairShawn M Burgess


Mammals are generally poor at tissue regeneration, often resulting in permanent damage (scarring) or complete loss of tissues, organs, and extremities following injury or as a natural consequence of ageing. In contrast, throughout their lifetime fish maintain a high capacity for regenerating complex tissues after injury. Studying these processes should provide insights into the pathways necessary to trigger therapeutic regeneration in humans. We utilize the zebrafish Danio rerio, which are able to regenerate many of their tissues and organs such as: the fin, retina, spinal cord, inner ear, and heart. In particular, the embryonic zebrafish tail serves as an ideal model of appendage regeneration due to its easy manipulation, relatively simple mixture of cell types, and superior imaging properties. Importantly, regeneration of the embryonic zebrafish tail requires development of a blastema, a mass of dedifferentiated cells capable of replacing lost tissue, which is a crucial step in all known examples of appendage regeneration. Using this model, we show that tail amputation triggers an obligate metabolic shift to glycolysis in cells comprising and surrounding the notochord during the repositioning of these cells near the amputatio...Continue Reading

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Mentioned in this Paper

Notochordal Canal
Blastema Predominant Wilms' Tumor
TGF-Beta Receptor Signaling Pathway
SNAI1 gene
Tissue Regeneration
Cell Type
FAM3C protein, human

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