Genetically Engineered Mice With Human Telomeres Offer New Aging Model
Scientists engineered mice with human-like telomeres, creating a powerful new model to study aging.
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Researchers at Washington State University (WSU) have developed genetically engineered mice with human-like telomeres, offering a new model for studying aging and disease. The findings, published in Nature Communications, could accelerate research on aging-related conditions and potential anti-aging treatments.
Telomeres and cellular aging
Aging occurs at the cellular level as telomeres – protective caps at the ends of chromosomes – gradually shorten. These structures function like shoelace tips, preventing genetic material from unraveling. Over time, telomere shortening limits a cell’s ability to divide, leading to cellular aging and eventual cell death.
Telomeres
Protective caps at the ends of chromosomes that prevent genetic material from degrading.Telomerase
An enzyme that helps maintain telomere length. In most human cells, telomerase is inactive after early development, but it remains active in cancer cells, allowing them to divide indefinitely.Mice typically have telomeres that are up to 10 times longer than humans, making it difficult to study human aging processes in traditional mouse models. The WSU research team, led by Jiyue Zhu from the College of Pharmacy and Pharmaceutical Sciences, developed a genetically engineered model in which mice have short, human-like telomeres and do not express telomerase – an enzyme that maintains telomere length – in adult tissues.
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“This is the first mouse model with truly humanized telomeres because telomerase isn’t expressed in adult tissues in this model. Our paper demonstrates that they exhibit human-like telomeres. Now, we aim to observe how these mice age.”
Dr. Jiyue Zhu.
A new model for studying aging and disease
The newly developed HuT mice (humanized telomere mice) enable researchers to study aging in an entire organism rather than in isolated human cells. The model provides opportunities to investigate how telomere length influences lifespan, age-related diseases and cancer.
One area of interest is how shorter telomeres reduce the risk of developing cancer. Rapidly dividing cancer cells require high levels of telomerase to maintain their telomeres. By studying HuT mice, researchers aim to understand how reducing telomerase activity in cancer cells could be a strategy for limiting tumor growth.
“This mouse model is quite different, as it allows us to observe the aging process in a whole organism. Mice are similar to humans in terms of organ structure, genes, and genetic makeup.”
Dr. Jiyue Zhu.
Expanding research applications
The HuT mice also allow researchers to explore the effects of environmental stress on telomere regulation. Christopher Davis, a researcher at the WSU Elson S. Floyd College of Medicine, is collaborating with Zhu’s team to examine how factors such as sleep deprivation influence aging at the cellular level.
The research builds on Zhu’s decades of work in telomere biology, which began in the 1990s under Nobel Prize-winning scientists Elizabeth Blackburn and J. Michael Bishop. Zhu and his team at WSU began developing the HuT mouse model 10 years ago after identifying key differences in telomere regulation between humans and animals.
Future directions
The WSU team plans to share HuT mice with other researchers studying aging, longevity, and cancer. With more than $5 million in grant funding from the National Institute on Aging, the National Institute of General Medical Sciences, and the U.S. Department of Defense, Zhu’s group aims to refine the model and investigate its implications for cancer treatments, including melanoma research.
By providing a tool that better simulates human aging, HuT mice may help scientists uncover new strategies to protect telomeres, slow cellular aging and develop therapies for age-related diseases.
Reference: Zhang F, Cheng D, Porter KI, et al. Modification of the telomerase gene with human regulatory sequences resets mouse telomeres to human length. Nat Comm. 2025;16(1):1211. doi: 10.1038/s41467-025-56559-6
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