the hair follicle, defects that may underlie delayed wound healing, hair greying and hair loss in these mice66. Even the brain, an organ of relatively low proliferative activity, shows a compromise of NSC renewal and differentiation capacity in late-generation Terc−/− mice63,67. The molecular pathways that sense telomere dysfunction and activate cellular checkpoint responses leading to these stem-cell defects and tissue degeneration phenotypes are not completely understood, although p53 has been shown to have a prominent role (see below).
