The fungus has essentially hacked its own genome
In the genomes of a lethal fungus, scientists have found that what was long dismissed as genetic noise is in fact a mechanism of amplified destruction. Researchers at the University of Exeter have shown that Batrachochytrium salamandrivorans — a pathogen linked to over 90 amphibian extinctions — exploits so-called jumping genes to multiply its own skin-destroying capabilities, turning a supposed evolutionary liability into a weapon. The discovery asks us to reconsider not only what we call 'junk,' but how quietly and ingeniously life reshapes itself in the pursuit of survival.
- A salamander-killing fungus has been found to carry nearly 19% repetitive DNA in its genome — a concentration that dwarfs the less-than-1% found in humans and defies conventional assumptions about genetic stability.
- By hijacking transposons — DNA sequences that copy and paste themselves — the fungus inadvertently amplifies nearby genes responsible for destroying salamander skin, making it a faster and more lethal pathogen than its relatives.
- European salamander populations, lacking the evolutionary defenses of their Asian counterparts, have been devastated by the fungus's spread, with the pathogen now implicated in over 90 amphibian extinctions worldwide.
- Scientists are now asking whether this genome-hacking strategy is far more common among pathogens than previously understood, and whether unraveling the mechanism could open new avenues for combating the fungus before further extinctions occur.
A fungus that preys on salamanders has turned what scientists once called genetic junk into an instrument of devastation. Researchers at the University of Exeter have found that Batrachochytrium salamandrivorans — known as Bsal — carries an extraordinary concentration of jumping genes, or transposons, that account for nearly 19% of its genome. In most organisms, including humans, these repetitive DNA sequences are kept tightly suppressed and represent less than 1% of the genetic code.
The danger lies in how transposons behave when they duplicate: they sometimes drag neighboring genes along with them. In Bsal's case, this molecular copying spree has repeatedly amplified the very genes responsible for breaking down salamander skin. Lead author Theresa Wacker described it as a blueprint where copied pages accidentally bring adjacent instructions with them — and in this pathogen, those instructions are for destruction. The result is a fungus that breaches its host's defenses far more rapidly than related species.
Bsal originated in Asia, where native salamanders have developed some tolerance to it over time. But when it reached Europe, it encountered populations with no such defenses, and the consequences have been catastrophic — driving salamander numbers into sharp decline and contributing to more than 90 amphibian extinctions globally.
Senior author Dr. Rhys Farrer noted that repetitive DNA has long been treated as an evolutionary remnant — disruptive, purposeless, and best suppressed. Bsal appears to be the exception: a pathogen that has effectively hacked its own genome, converting genetic instability into amplified virulence. The finding raises a broader and unsettling question — if this strategy confers such a clear advantage, how many other pathogens may be quietly exploiting the same mechanism? The team is now investigating whether transposon-driven genome expansion is more widespread than science has yet recognized, and whether that knowledge might one day be turned against the fungus itself.
A fungus that preys on salamanders has found an unexpected evolutionary advantage in what scientists once dismissed as genetic junk. Researchers at the University of Exeter have discovered that Batrachochytrium salamandrivorans—a pathogen responsible for more than 90 amphibian extinctions worldwide—carries an unusually high concentration of jumping genes, or transposons, that allow it to copy and paste itself throughout its genome with devastating effect.
Jumping genes are DNA sequences that can duplicate themselves, moving around within an organism's genetic code. Most living things carry some of these repetitive elements, but they typically keep them in check. In humans, they account for less than 1% of the genome. Bsal, as the fungus is abbreviated, has taken a radically different path. Nearly 19% of its genome consists of these jumping genes—a concentration that should, by conventional understanding, be a liability. Yet the fungus appears to have weaponized this genetic redundancy.
The mechanism works through a kind of molecular photocopying gone haywire. When transposons duplicate themselves, they sometimes capture and amplify nearby genes in the process. In Bsal's case, this copying spree has multiplied genes responsible for destroying salamander skin. The result is a pathogen that can breach and devastate its host's protective barrier far more rapidly than related fungal species. Theresa Wacker, the study's lead author, explained the process by analogy: if a genome were a blueprint, transposons would be identical pages that, when copied, sometimes bring adjacent pages along for the ride. In Bsal, those extra pages happen to contain the instructions for skin destruction.
The fungus emerged in Asia, where native salamanders and newts have evolved some tolerance to it. But when Bsal reached Europe, it found populations with no such defenses. European salamander numbers have plummeted as the pathogen spread across the continent. The skin infections it causes are severe and often fatal, turning what might have been a manageable threat into an extinction event.
Dr. Rhys Farrer, the study's senior author, noted that repetitive DNA has long been dismissed as junk—a evolutionary remnant with no purpose. The conventional wisdom held that organisms would naturally suppress such sequences because they risk disrupting normal gene function. Bsal seems to have found the exception to that rule. For this particular pathogen, the advantages of amplified virulence outweigh any costs of genetic instability. The fungus has essentially hacked its own genome, turning a supposed weakness into a competitive edge.
The discovery raises unsettling questions about how common this strategy might be in nature. If jumping genes can confer such a clear evolutionary advantage to a pathogen, why aren't more disease-causing organisms exploiting the same mechanism? Farrer suggested that genome expansion through transposon activity is probably far more widespread than current research has revealed. The team is now investigating whether similar patterns appear in other pathogens, and whether understanding this mechanism might eventually lead to new ways of combating the fungus. For now, the finding represents a fundamental shift in how scientists think about repetitive DNA—no longer junk, but a potential driver of pathogen evolution and virulence.
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If you think of an organism's genome as a blueprint, transposons are like having many identical pages. And sometimes, during the process of copying and pasting, other parts of the book are also copied.— Theresa Wacker, study first author, University of Exeter
This kind of gene repetition is probably more widespread in nature than we currently realize. If it confers an evolutionary advantage for the pathogen by making it more virulent, it's not clear why this isn't much more common.— Dr. Rhys Farrer, senior author
A Conversa do Hearth Outra perspectiva sobre a história
So the fungus is using these jumping genes to make itself more dangerous. But why would that work? Wouldn't a genome full of copies be unstable?
You'd think so. In most organisms, having 19% of your genome be repetitive sequences would be a mess—genes stepping on each other, normal functions breaking down. But Bsal seems to have found a sweet spot where the chaos is actually useful. The copying process amplifies the genes that destroy salamander skin, and that advantage outweighs any cost.
It sounds like the fungus accidentally discovered a loophole in evolution.
Not quite accidentally. Once those extra skin-destroying genes were in place, natural selection would favor the strains that had more of them. The fungus didn't plan it, but the mechanism—the jumping genes doing their copying—created the variation that selection could act on.
And this is why it's so deadly to European salamanders specifically?
Exactly. Asian salamanders have had time to develop some tolerance. But European populations never encountered this pathogen before. They have no defenses against something that can breach their skin so efficiently. It's like introducing a predator to an island where nothing has learned to fear it.
The researchers seem surprised this isn't more common. Why would other pathogens ignore such an obvious advantage?
That's the real mystery. Maybe it is more common and we just haven't looked closely enough. Or maybe there's a cost we don't fully understand yet—something about genome instability that only works for this particular fungus in this particular ecological niche. The researchers are essentially saying: we found one example of this working brilliantly. Now we need to figure out if it's a fluke or a pattern.