How a Missing Gene Speeds Up Aging: New Insights into Telomere Health
Scientists from the German Mouse Clinic at the Institute of Experimental Genetics (Helmholtz Munich) have studied the effects of a missing gene, Ten1, on aging. By generating a mouse model with Ten1 deficiency, researchers observed that without this gene, mice age faster and their chromosomes’ protective caps – called telomeres – become significantly shorter. These findings mirror symptoms of Dyskeratosis Congenita, a rare genetic disorder that affects telomere maintenance. The study was conducted with collaborators from DZNE (Bonn, Germany), CNIO (Madrid, Spain) and NCI (Bethesda, USA).
Telomeres act like tiny shields at the ends of our chromosomes, preventing damage and ensuring cell health. As we age, telomeres naturally shorten, but when this process speeds up, it can cause early aging and disease. In the study, researchers found that mice lacking TEN1 not only had shorter telomeres but also fewer dividing cells, more cell death, and a loss of vital stem cells. This was linked to the activation of a stress response in the body, specifically the p53/p21 pathway, which plays a role in aging and cell survival.
“For the first time, we show how TEN1 directly influences telomere stability inside an animal,” says study lead Martin Hrabě de Angelis. “Without it, cells struggle to repair themselves, leading to early aging. Understanding this process brings us one step closer to uncovering the deeper molecular mechanisms behind aging.”
Beyond deepening our understanding of aging, this study could contribute to the development of treatments for telomere-related diseases – also known as Telomere Biology Disorders (TBDs) – as well as other age-associated conditions.
Original Publication
Sanz-Moreno, Becker, Xie et al., 2025: Loss of Ten1 in mice induces telomere shortening and models human dyskeratosis congenita. Science Advances. DOI: 10.1126/sciadv.adp8093
