Epimorphic Regeneration in Mice Is p53-Independent

The study explored the role of the p53 protein in the regenerative process of ear hole closure in MRL mice, a model for mammalian epimorphic regeneration. It was found that the absence of p53 did not hinder the healing ability of MRL mice; in fact, these mice showed an increased level of adipocytes and chondrocytes in the healing tissue compared to MRL or p21-null mice. The research also indicated that other cell cycle-related proteins, such as p16 and Gadd45, are important for regeneration, as mice lacking these proteins exhibited little healing. The study suggests that p53 signaling is not essential for mouse appendage regeneration and that p21 may be involved in the regenerative process through a p53-independent pathway, potentially involving the Tgfß/Smad pathway. The findings imply that p53-induced senescence is not a requirement for tissue regeneration in this model, and that the interaction between p53 and p21 in MRL mice may be defective.