5/6) This is evolution’s trade-off in genetic form: one gene helping build a faster, more fertile youth while increasing the risk of disease later. The next challenge is profound: can biology keep the vigor, but lose the cost?
6/6) Spearheaded by Dr. Marva Bergman, with wonderful collaboration from @ayoubnlab and @AlexeiMaklakov
. “An Antagonistically Pleiotropic Gene Regulates Vertebrate Growth, Maturity, and Lifespan” is now in
@NatureComms: www.nature.com/articles/s41...
4/6) The lifespan cost was clear: male vgll3 mutants had a 15% shorter median lifespan and a 55% higher risk of death. The gene also altered DNA-damage responses, a central fault line in aging biology.
2/6) The bargain paid early. Male mutants grew faster, matured sooner, and showed more proliferating germline and intestinal stem cells. Their bodies seemed to press fast-forward on youth.
3/6) Then came the bill. As mutant males aged, they developed more melanoma-like tumors. Using a new immunodeficient killifish model, we showed these tumor cells could engraft and invade.
1/6) What if aging begins, in part, as a bargain made in youth? In turquoise killifish, editing vgll3—a gene linked to puberty-timing in humans and salmon—revealed one of the first causal single-gene examples of antagonistic pleiotropy in vertebrate aging 🧵
Itamar Harel
Itamar Harel
Itamar Harel
Itamar Harel
Itamar Harel
Itamar Harel
Here they use killifish to reveal a stark genetic trade-off in aging. They found that disrupting the vgll3 gene accelerates early-life maturation and growth but directly increases the risk of age-rela...
