Blood-cell telomerase delays premature aging in zebrafish

In an animal experiment, researchers studied zebrafish lacking Rag1, a gene needed for adaptive immunity. These fish develop premature aging marked by gut degeneration, systemic inflammation, and an imbalance in gut bacteria. Depleting the gut bacteria rescued survival and reduced inflammation. Transferring microbes from the mutant fish into healthy zebrafish transmitted mutant-like molecular features, establishing the bacterial imbalance as a causal amplifier of the condition. The team also tested telomerase, an enzyme that maintains chromosome caps called telomeres. Genetic loss of telomerase accelerated death. In contrast, increasing telomerase specifically in blood-forming cells extended lifespan. It reprogrammed gene activity in blood cells and partly restored gut, liver, and bacterial balance, without major changes in telomere length.