Hebrew University Links vgll3 to Faster Growth and Shorter Lifespan in Killifish
Updated
Updated · SciTechDaily · Jun 21
Hebrew University Links vgll3 to Faster Growth and Shorter Lifespan in Killifish
2 articles · Updated · SciTechDaily · Jun 21
Summary
CRISPR-edited African turquoise killifish carrying altered vgll3 grew faster, matured earlier and then died sooner, giving vertebrate evidence for an evolutionary youth-versus-longevity trade-off.
The same fish developed more age-related tumors, including melanoma-like cancers, as researchers tied vgll3 to cell division, stem-cell activity and DNA repair.
Hebrew University-led scientists said the findings help explain how early-life biological advantages can later drive aging and disease rather than long-term body maintenance.
Because vgll3 is also present in humans, the team said the work could inform research on puberty, cancer and healthier aging; they next aim to separate the gene's benefits from its late-life harms.
If cancer is the evolutionary price for early fertility, is targeting this 'youth' gene the future of medicine?
Nature designed us to 'sprint, not marathon.' Can new gene-editing tools finally let us win both races?
VGLL3: The Genetic Trade-Off Between Early-Life Growth and Late-Life Cancer Risk
Overview
In June 2026, Professor Itamar Harel and his team made a breakthrough by showing that the vgll3 gene is a central regulator of growth, maturation, aging, and cancer risk in African turquoise killifish. Using CRISPR gene editing, they disrupted vgll3 and observed major changes in the fish’s development and lifespan. Their experiments confirmed antagonistic pleiotropy: vgll3 gives early-life advantages but causes harm later, such as increased tumor risk. This dual role reveals a trade-off between rapid growth and long-term health, offering new insights into how genes shape aging and disease in both fish and humans.