Telomere changes are associated with disease, such as dyskeratosis congenita (DKC). Patients with DKC suffer from premature aging, bone marrow failure and a predisposition to cancer associated with impaired telomerase, disrupting normal telomere maintenance. Marie Meznikova and colleagues made a mouse with one functional allele of telomerase reverse transcriptase (Tert), a telomere-replenishing factor that maintains telomeres. Interbreeding of mTert-haploinsufficient mice for several generations restores telomerase function, suggesting corrective mechanisms for future telomere lengthening in mammals. Evoking these restorative pathways in human patients with DKC might limit some of the pathological effects of telomere shortening.
