01 Jun Gene That Speeds Growth and Maturity Also Shortens Lifespan: New Evidence for Evolutionary Trade-Off in Aging

MedicalResearch.com Interview with: Prof. Itamar Harel PhD,  Hebrew University
The International team was led by Dr. Eitan Moses, Dr. Marva Bergman, and Prof. Itamar Harel at Hebrew University, in collaboration with Prof. Nabieh Ayoub (Technion) and Prof. Alexei A. Maklakov (University of East Anglia)

MedicalResearch.com: What is the background for this study? What are the main findings?
Response: A major question in aging biology is why some animals “live fast,” mature early, and age quickly, while others mature slowly and live much longer. One evolutionary idea, called antagonistic pleiotropy, suggests that some genes may help animals early in life but harm them later.

We studied vgll3, a gene previously linked by genome-wide association studies* to puberty timing in humans and maturation in Atlantic salmon. Using CRISPR gene editing in the short-lived African turquoise killifish, we found that altering vgll3 accelerated male growth and sexual maturity, or slow it down (depending on which isoform we manipulated). However, this early-life advantage came with a cost: older mutant males developed more melanoma-like tumors and had shorter lifespans.

In simple terms, vgll3 appears to tune the pace of life – linking growth, reproduction, cancer risk, and aging.

* Genome-wide association studies, or GWAS, are studies that scan the genomes of many individuals to identify genetic variants associated with traits or diseases.

Dr. Eitan Moses

MedicalResearch.com: Can the vgll3 gene be modulated to be expressed differently at different times or in different tissues?
Response: Our study suggests that vgll3 is naturally regulated in several ways. It has different isoforms, and its expression is enriched in specific male gonadal support cells, including Sertoli and Leydig cells.

We did not yet directly switch vgll3 on or off at specific ages or in specific tissues. That is an important future goal. Time- or tissue-specific control would help test whether the early benefits of vgll3 modulation can be separated from its late-life costs.

MedicalResearch.com: What should readers take away from your report?
Response: Aging is not only about damage accumulating over time. It is also connected to the same biological programs that regulate development, growth, reproduction, stem-cell activity, and tissue renewal.

Our study provides causal evidence that one conserved gene can speed up early-life traits while increasing late-life disease risk. This supports the idea that aging can emerge, at least in part, from evolutionary trade-offs: nature may favor early reproductive success even when it carries costs later in life.

MedicalResearch.com: What recommendations do you have for future research?
Response: Future work should determine exactly how vgll3 affects cell proliferation, hormone signaling, DNA repair, and cancer risk.

It will also be important to test whether vgll3 acts differently depending on age, tissue, sex, or isoform. A major goal will be to ask whether healthy growth and reproductive timing can be biologically separated from late-life cancer risk and aging.

Finally, studies in wild populations and other vertebrates could reveal whether similar mechanisms help explain natural differences in maturation, lifespan, and age-related disease.

MedicalResearch.com: Is there anything else you would like to add? Any disclosures?
Response: This study builds on our broader work showing that reproduction, repair, metabolism, and lifespan are deeply connected in vertebrates. Our previous work showed that different forms of germline manipulation can have sex-specific effects on repair and longevity.

The study also generated a new immunodeficient killifish model, which allowed us to transplant and study tumor cells in this emerging aging model.

These findings are basic biology and should not be interpreted as a medical recommendation to target VGLL3 in humans. The authors declare no competing interests.

Citation:
The research paper titled “An Antagonistically Pleiotropic Gene Regulates Vertebrate Growth, Maturity, and Lifespan” is available in Nature Communications and can be accessed at DOI:10.1038/s41467-026-72381-0.

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Last Updated on June 3, 2026 by Marie Benz MD FAAD