Researchers have identified a gene that appears to balance a powerful evolutionary trade-off, boosting growth and reproductive success early in life while carrying hidden costs later on.
The biological processes that help build a healthy young body may also sow the seeds of aging and cancer. Researchers have now identified a gene that appears to do exactly that, driving rapid growth and early reproductive success while increasing the risk of disease and shortening lifespan later in life.
The discovery provides some of the strongest experimental evidence to date for antagonistic pleiotropy, a long-standing evolutionary theory proposing that genes beneficial in youth can have harmful effects in old age. The study was led by Dr. Eitan Moses, Dr. Marva Bergman, and Prof. Itamar Harel of Hebrew University in collaboration with Prof. Nabieh Ayoub (Technion) and Prof. Alexei A. Maklakov (University of East Anglia).
Despite decades of research, scientists have struggled to pinpoint the genes behind these evolutionary trade-offs in vertebrates. The team investigated vgll3 in the African turquoise killifish, a species widely used to study aging because of its naturally short lifespan. Previous studies had linked the gene to the timing of puberty and maturation, but its broader role in shaping lifespan and disease risk remained unclear.
vgll3 Drives Faster Growth and Earlier Reproduction
Using CRISPR gene-editing technology, the researchers altered vgll3 and observed major changes. Fish carrying the modified gene grew more quickly and reached sexual maturity sooner, characteristics that could improve reproductive success in the wild.
Those advantages came at a cost. The same fish lived shorter lives and developed more age-related tumors, including cancers resembling melanoma.
“We have effectively caught evolution in the act of making a trade-off. For years, we’ve asked why our bodies can’t just maintain themselves indefinitely. This gene gives us a direct answer: nature doesn’t prioritize longevity; it prioritizes continuity. We are built to sprint, not to marathon,” said Dr. Harel.
How Growth Mechanisms Increase Cancer Risk
Additional experiments revealed that vgll3 affects several important biological functions, including cell division, stem cell activity, and DNA repair. Higher levels of cellular activity may help explain why the fish developed more rapidly when young while also accumulating damage that later contributed to disease.
The team also created a new immunodeficient killifish model, allowing researchers to transplant and study tumor cells in ways that were not previously possible in this species.
“What’s fascinating—and slightly terrifying—is that the cancer we see in these fish isn’t a random accident. It’s the direct shadow of their youthful vitality. The same machinery that drives a cell to build a young body is hijacking the system to build a tumor in the old one. If we can understand this mechanism, we might finally learn how to decouple healthy growth from the disease of aging,” Dr. Harel added.
Human Aging and Cancer Research Implications
Because vgll3 is also found in humans, the results could help scientists better understand human development, aging, and age-related diseases. Earlier studies linked the gene to puberty timing and hormone levels, but direct evidence of its biological function had been lacking.
The discovery may aid future efforts to prevent cancer and extend healthy lifespan. Researchers say their next goal is to determine whether the gene’s early-life benefits can be separated from the harmful effects that emerge later in life.
Reference: “An antagonistically pleiotropic gene regulates vertebrate growth, maturity, and lifespan” by Eitan Moses, Marva Bergman, Tehila Atlan, Elizabeth M. L. Duxbury, Roman Franěk, Omer Ben Dor, Henrik von Chrzanowski, Enas R. Abu-Zhayia, Nabieh Ayoub, Shay Kinreich, Ido Ben-Ami, Alexei A. Maklakov and Itamar Harel, 2 June 2026, Nature Communications.
DOI: 10.1038/s41467-026-72381-0
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