LeClaire Institute

Insights into longevity and virus-driven adaptation from Myotis bat genomes

Juan M Vazquez, M Elise Lauterbur, Saba Mottaghinia … Peter H Sudmant

Nature · 26 Aug 2026 · Research

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Read the original paper →doi:10.1038/s41586-026-10932-7

Open access. The full paper is free to read.

Near-complete genomes of eight bat species link their long lives to adaptations in cancer pathways and an unusual response to DNA damage.

Why it matters

Some small bats live far longer than expected for their size, and they also tolerate viruses unusually well. Comparing closely related bats with very different lifespans is a powerful way to find genes linked to long life. This study connects longevity, cancer resistance and DNA-damage responses in one group of mammals. Long-lived species are, in a sense, natural experiments that have already solved part of the aging problem, which is why comparative studies like this one, and the bowhead whale study above, look for repair and cancer-defence genes.

What they did

The researchers generated cell lines and near-complete genome assemblies for eight closely related Myotis bat species. They ran genome-wide screens for positive selection, analysed structural variation such as gene duplications, and did experiments in primary cells, including tests of the DNA-damage response in the long-lived little brown bat, Myotis lucifugus.

What they found

Bats showed different modes of adaptation to DNA and RNA viruses than other mammals: positive selection was over-represented in proteins that interact with DNA viruses, and copy-number changes were more common in proteins that interact with RNA viruses. The immune gene EIF2AK2 (PKR) had multiple ancient duplications shared across species. The repeated evolution of long life in Myotis was associated with positive selection in cancer pathways, and cells of the long-lived Myotis lucifugus showed a unique response to DNA damage. The authors suggest that bats' longevity and immunity are linked through adaptations to viruses and to aging-related disease.

Limits

Evolutionary signals show which genes changed, not exactly how those changes extend life. The DNA-damage experiments were done in cultured cells from one species. The abstract does not describe the DNA-damage response in detail or test whether it extends lifespan. Bats also differ from humans in body temperature, flight and hibernation, any of which could interact with these genes. The study points to candidate pathways for future testing rather than ready-made treatments.

Key terms

Positive selection
Evolution favouring changes in a gene because they help survival or reproduction.
Genome assembly
A reconstructed, ordered sequence of a species' DNA.
Copy-number variation
Differences in how many copies of a gene a genome carries.
DNA-damage response
The cell's system for detecting DNA damage and deciding whether to repair it, pause, or die.
Primary cells
Cells taken directly from an animal rather than a long-term lab line.
EIF2AK2 (PKR)
An immune protein that senses viral RNA and shuts down protein production in infected cells.
Structural variation
Large changes in the genome, such as duplicated or deleted genes.

Sources and signals

This synopsis was written from the published abstract only. Key terms are general definitions added for readers.