A new study identifies vgll3 as a key gene that promotes rapid growth and early reproduction while increasing the risk of aging and cancer later in life. The discovery provides rare experimental evidence for the theory that evolution favors early childhood advantages, even at the expense of long-term health. Researchers say the discovery could open new avenues for understanding and potentially separating biological links between development, aging and disease.
Researchers have identified genes directly associated with early growth and reproductive success, as well as accelerated aging and increased cancer risk later in life, providing new insight into a long-standing theory in evolutionary biology.
Now, an international team led by Dr. Eitan Moses, Dr. Marva Bergman and Professor Itamar Harel from the Hebrew University, in collaboration with Professor Navier Ayoub (Technion) and Professor Alexei A. Maklakov (University of East Anglia), has provided experimental evidence for the antagonistic pleiotropy theory, the idea that certain genes contribute to disease and decline in old age, while conferring benefits early in life.
Although widely accepted in theory, scientists have struggled to identify the specific genes responsible for such trade-offs in vertebrates. Using the African turquoise killifish, a short-lived species recently pioneered by Harrell and colleagues to study genetic aging, the research team focused on genes. vgll3which has previously been linked to the timing of puberty in humans and maturation in other species, particularly Atlantic salmon.
Researchers observed clear effects by modifying this gene using CRISPR technology. changed fish vgll3 This trait of growing faster and reaching sexual maturity earlier may confer reproductive advantages in the natural environment.
However, these benefits came at significant costs in the long run. The same fish had shorter lifespans and higher rates of age-related tumors, including cancers like melanoma.
We have effectively captured evolution in the act of trade-offs. For years, we’ve wondered why our bodies can’t stay the way they are forever. This gene gives us a direct answer. Nature does not prioritize longevity. Prioritize continuity. We are built to run sprints, not marathons. ”
Professor Itamar Harel, Hebrew University
Further analysis showed that this gene influences important biological processes, including cell division.
Stem cell activity and DNA repair. Increased cellular activity may help explain both rapid changes.
Young fish show growth, while older fish show an accumulation of damage that can lead to disease.
The researchers also developed a new immunodeficient medaka model, allowing them to implant and study tumor cells in ways not previously possible with this system.
“What’s interesting, and a little scary, is that the cancers we see in these fish are not accidental accidents; they are a direct shadow of their youthful vitality. The same machinery that drives cells to create young bodies is also hijacking the systems that create tumors in older bodies. Understanding this mechanism may ultimately tell us how to separate healthy growth from the diseases of aging,” added Dr. Harrell.
because vgll3 is conserved in humans, and this discovery could have far-reaching implications for our understanding of human development, aging, and age-related diseases. Previous studies have linked this gene to pubertal timing and hormone levels, but functional data have been lacking until now.
The findings could contribute to future efforts in research aimed at preventing cancer and extending healthy lifespans. The next step, the researchers say, will be to investigate whether it is possible to distinguish between a gene’s initial beneficial effects and its later harmful effects.
sauce:
Hebrew University of Jerusalem
Reference magazines:
Moses, E. others. (2026). Antagonistically pleiotropic genes regulate growth, maturation, and lifespan in vertebrates. Nature Communications. DOI: 10.1038/s41467-026-72381-0. https://www.nature.com/articles/s41467-026-72381-0
