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Itamar Harel

@itamarh.bsky.social
28 followers 1 following 6 posts

Associate Professor, Genetics @ the Hebrew University, and a dad. Experimental biology of vertebrate aging and related diseases using the killifish model

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Itamar Harel @itamarh.bsky.social · 02/06/2026
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...
nature.com
An antagonistically pleiotropic gene regulates vertebrate growth, maturity, and lifespan - Nature Communications
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...
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Itamar Harel @itamarh.bsky.social · 02/06/2026
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?
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Itamar Harel @itamarh.bsky.social · 02/06/2026
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.
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Itamar Harel @itamarh.bsky.social · 02/06/2026
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.
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Itamar Harel @itamarh.bsky.social · 02/06/2026
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.
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Itamar Harel @itamarh.bsky.social · 02/06/2026
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 🧵
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