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Fig. 7
(A) In homeostasis, mature OBs reside in close contact with the bony-ray surface, secreting the collagenous bone matrix. (B) Upon caudal fin amputation, OBs and other cell types in the regenerating fin respond by undergoing a metabolic adaptation that stimulates glycolysis and is essential for regeneration to proceed. Enhancing glycolytic influx promotes OB dedifferentiation, by releasing Cyp26b1 from NF-ΚB repression, and cell cycle re-entry, by interfering with the master regulation of caudal fin proliferation Fgf20a, thereby enabling OBs to act as progenitor cells. Moreover, glycolysis is necessary to maintain the correct proliferative ability and distribution of OBs populations within the blastema, during its formation. (C) Glycolysis inhibition has a severe impact on OB dedifferentiation and pre-OBs pool assembly, which supports new OB formation and proliferation, ultimately leading to impaired bony-ray regeneration and suppression of blastema formation.