One Splicing Gene Added 14% to Old Mice's Median Lifespan

Jeff's Daily Pick. Switching on one RNA splicing gene, SRSF1, in old female mice raised median lifespan from 778 to 886 days, about 14% (Nature Aging). Only 10 treated mice and 9 controls, and no human treatment exists.

In the United States, a team led by George Church at Harvard's Wyss Institute and Antonio del Sol published a study in Nature Aging on October 14, 2026 that looked for single genes able to make old cells look young again. The starting point was a known problem: the Yamanaka factors can reset aged cells, but they also erase cell identity and carry a tumor risk, which limits their use in living animals.

How the gene was found

The researchers first built a transcriptomic age predictor, a model that estimates the age of human skin fibroblasts from the genes they express. They then switched on hundreds of candidate genes one by one and scored which ones pushed old cells toward a younger profile. The top hit was SRSF1, an RNA processing and splicing factor. In the dish, it lowered markers of senescence, protein stress and inflammatory signaling while the cells stayed fibroblasts. In worms, knocking down the SRSF1 equivalent blocked the long life of a long lived mutant strain.

The mouse numbers

In aged mice, the team packed the mouse gene into a virus that mainly reaches the liver, with a drug controlled switch to turn it on. According to the paper's abstract, inducible SRSF1 expression cut the progression of frailty by 44% and was associated with a 14% longer median lifespan, with 9 to 10 mice per group. As reported by The Brighter Side of News from the paper, the lifespan test used 10 treated female mice and 9 controls, the gene was delivered at 561 days of age and switched on at 606 days, and median lifespan reached 886 days against 778 for controls. That is 108 extra days, or 13.9% of the control median.

Not every test worked. In the paper's extended data, faster wound healing depended on how the gene was delivered, and one muscle regeneration deficit in old mice was not rescued by a constantly active version. The result is a target worth testing, not a treatment. Our piece on metabolic aging clocks covers another way researchers try to measure biological age, and two enzymes and memory in aging mice is a recent example of how far mouse results sit from the clinic.