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The death of different types of cells occurs in regressing or remodeling organs to transform from a tadpole to a frog in both temporally and spatially regulated manners during amphibian metamorphosis. This morphological change is drastic and visible with the naked eye. This review summarizes our current understanding of the basic mechanism of the cell death during the metamorphosis. It focuses in particular on the tail resorption and the remodeling of intestine and skin where programmed cell death is executed by thyroid hormone-signaling through the cell-autonomous response (suicide) and the degradation of the extracellular matrix (murder).
Fig. 1.
The developmental morphological changes of a single tadpole during the climax of metamorphosis. A single tadpole of Xenopus laevis is photographed at the various stages. It is worth noting that the head region, dorsal muscle and a tail decrease in size, as the metamorphosis proceeds.
Fig. 2.
Comparison of the murder model and the suicide model. Green and yellow squares indicate DNTR-expressing and non-transfected muscle cells, respectively, and white rectangles mean subepidermal fibroblasts. Thyroid hormone (light blue ovals) induces these cells to release the death factor or the extracellular matrix-degrading protease (orange circles) outside cells in the murder model or to produce suicide protein (blue circles) in the suicide model. The basement membrane (red region) between muscle cells is dissolved by the protease secreted by subepidermal fibroblasts and muscle cells.
Fig. 3.
The process of tail muscle cell death during amphibian metamorphosis. Green rhomboids represent transfected muscle cells in a tail injected with control vector (A) or DNTR expression construct (B), while yellow ones are non-transfected muscle cells. At NF stage 63, the notochord (blue) is degenerated, and muscle cells change the shape.