The team showed that p21, a cell cycle regulator, was found to be consistently inactive in cells from MRL mice. When they looked at p21 knockout mice, they found that, unlike normal mice which heal wounds by forming a scar, mice that lack p21 begin by forming a blastema, a mass of cells capable of rapid growth and de-differentiation which behave more like embryonic stem cells than adult mammalian cells. The p21 knockout mice were able to replace missing or damaged tissue with healthy tissue that showed no signs of scarring.
Since the cyclin-dependent kinase p21 is one of the best characterized downstream targets of the tumour suppressor p53, knockout of p21 might be expected to increase the incidence of cancer and other studies have suggested that p21-deficient mice develop tumours at an earlier age than their wild-type counterparts and are more susceptible to the effects of some carcinogens. Although increased DNA damage was observed in the present study, there was also an increased incidence of apoptosis and no net increase in the incidence of cancer. If MRL mice and p21 knockout mice are a good model for tissue regeneration in humans, temporary inactivation of the p21 gene could eventually be used to speed up wound healing in people.
The study is published in PNAS.