Science1 publisher3 min readPublished
The little brown bat's cells answered a lethal dose by turning up cell-death genes
A Berkeley team's first analysis of eight Myotis genomes, out in Nature, links longer bat lifespans to higher levels of cancer-fighting genes. The same lab's dish experiments point at how damaged cells get cleared.
The Scientist · Science desk
What happened
- A team led by Juan Manuel Vazquez at UC Berkeley published the first analysis of eight genomes from the bat genus Myotis in the journal Nature.
- The comparison found that longer-lived species carried higher levels of genes associated with fighting cancer, which the authors read as a strong connection between lifespan and immune function.
- The same analysis found substantial overlap between the genes associated with aging and the genes involved in defending against disease.
- Cultured wing cells from Myotis lucifugus, the longest-lived bat in the sample, met a lethal chemical dose by raising the activity of cell-death genes instead of DNA repair genes.
- One Brandt's myotis, banded in Europe, was recaptured 50 years later, an individual record that anchors how long some Myotis species survive at their body size.
Compiled by The ScientistSomething wrong?How this is made
Why it matters
- constraint A correlation across eight species in one genus cannot separate a single ancestral change from several independent ones, so the immune-lifespan link stays a hypothesis until wider sampling tests it.
- capability The living cell collection lets the damage-response experiment be repeated in species that were never sequenced. That is how anyone would learn whether the death-first response is general among long-lived bats.
- decision Aging researchers get a target hypothesis out of this, immune upkeep together with clearance of damaged cells, and any human claim requires experiments in human cells that nobody has reported here.
- precedent If Vazquez's elephant comparison holds up under a matched assay, clearance of damaged cells becomes a candidate route to cancer resistance in animals of very different size, alongside better repair.
Eight species is a thin denominator for a question about lifespan, and the eight sit inside one genus [12]. Species that close together share recent ancestry, so a pattern that arose once in a long-lived branch can show up in several species without having evolved several times. The Berkeley release does not report effect sizes, statistical tests or per-species sample sizes [18]. Taken as written, the finding is a ranking within Myotis: the longer-lived species carried higher levels of genes associated with fighting cancer [2].
Vazquez takes the finding further than that ranking. "Bats evolved to live for a long time without getting diseases, which suggests that we don't necessarily need to look at diseases of aging and diseases of infection as completely separate fields," he said [14].
The dish experiments come with a manipulation. Vazquez grew cells from wing biopsies, exposed them to toxic chemicals at a lethal dose, and read out which genes switched on [4]. "We found the literal opposite of what we expected if you treat the bats with a lethal dose of this chemical," he said [6].
He put the elephant in the same category. "The longest-lived bat in North America decides 'I can't save this ship' and immediately switches gears to prioritize killing off the cells that are damaged. The elephant, another cancer-resistant species that is long-lived, has the exact same strategy -- if you can't save the cell, kill the cell," Vazquez said [7]. The elephant half of that is his reading of an animal outside this study. The assay itself ends at the dish, with gene activity in cultured cells as the readout [5].
The paper used a fraction of Vazquez's cell collection. He keeps cultures from 259 individuals representing 32 species [8], which is four times the number of species sequenced [15] and averages about eight individuals per species [16]; the cells come from bats caught in mist nets over Western streams and ponds and released after biopsy [9]. Running the same toxin assay across those species would show whether killing damaged cells tracks lifespan inside the genus, or whether Myotis lucifugus is one species with its own solution.
I would treat the death-over-repair result as the more testable of the two findings, because a dose response is something another lab can copy at the bench.
Peter Sudmant, a Berkeley associate professor of integrative biology who studies the genetics of aging and lifespan, described the aim this way: "By looking across the diversity of life and the remarkable longevities of different species, we hope we can better understand the interplay between DNA damage and the immune system to enable us to have full and healthy life spans" [11]. The human application, in the release's own framing, is a hope that these genetic tricks could eventually reveal new ways to protect health during aging [17].
What to watch
- Whether the Nature paper's statistics hold the lifespan-immunity association once shared ancestry among Myotis species is accounted for.
- Whether the toxin assay, repeated across the 32 cultured species, finds cell-death-first responses in other long-lived bats.
- Whether any lab runs bat, elephant and human cells side by side at the same dose of the same chemical.