Splicing factor SRSF1 slows aging in worms and mice
What if you could roll back the biological age of a cell without erasing its identity? That may sound far-fetched, but researchers have taken a step in that direction. A protein involved in reading DNA turns out to play a surprising role in aging.
Scientists conducted a large-scale screening study, testing hundreds of factors for their ability to rejuvenate the transcriptome (the full set of active genes in a cell) without changing the cell’s type. The protein that emerged from this search was SRSF1: a splicing factor, meaning a protein that helps determine which parts of the genetic blueprint are actually used. The study, published in Nature Aging, shows that SRSF1 lowers the transcriptomic age of cells in culture, and that higher activity of this protein is associated with slower aging in both worms and mice.
What is a splicing factor?
Genes are not directly converted into proteins inside cells. An intermediate step is involved: the RNA messenger is edited, with some sections kept and others discarded. This editing process is called splicing. SRSF1 is one of the proteins that controls it. During aging, this process becomes less precise, leading to greater variability in gene activity between cells. SRSF1 appears to stabilise it.
Cautious optimism
The study is impressive in scope: the screen covered many factors, and findings were validated across multiple models. Even so, caution is warranted. This involves cell cultures, worms and mice, not humans. Whether manipulating SRSF1 in people is safe and effective remains to be studied.
What makes the finding notable for longevity science is the suggestion that the transcriptome does not age irreversibly. A molecular switch may be able to slow this process without erasing the cell’s identity, opening a direction for future aging therapies.
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