Next, Kapusta calculated how much ancestral DNA each lineage had lost and how much new material it had gained. As she and Feschotte suspected, the bat lineages had churned through base pairs, dumping more than 1 billion while accruing only another few hundred million. Yet it was the other mammals that made their jaws drop.

Mammals are not especially diverse when it comes to genome size. In many animal groups, such as insects and amphibians, genomes vary more than a hundredfold. By contrast, the largest genome in mammals (in the red viscacha rat) is only five times as big as the smallest (in the bent-wing bat). Many researchers took this to mean that mammalian genomes just don’t have much going on. As Susumu Ohno, the noted geneticist and expert in molecular evolution, put it in 1969: “In this respect, evolution of mammals is not very interesting.”

Aurélie Kapusta, a research associate in human genetics at the University of Utah and the USTAR Center for Genetic Discovery. Mary-Anne Karren

But Kapusta’s data revealed that mammalian genomes are far from monotonous, having reaped and purged vast quantities of DNA. Take the mouse. Its genome is roughly the same size it was 100 million years ago. And yet very little of the original remains. “This was a big surprise: In the end, only one-third of the mouse genome is the same,” said Kapusta, who is now a research associate in human genetics at the University of Utah and at the USTAR Center for Genetic Discovery. Applying the same analysis to 24 bird species, whose genomes are even less varied than those of mammals, she showed that they too have a lively genetic history.

“No one predicted this,” said J. Spencer Johnston, a professor of entomology at Texas A&M University. “Even those genomes that didn’t change size over a huge period of time—they didn’t just sit there. Somehow they decided what size they wanted to be, and despite mobile elements trying to bloat them, they didn’t bloat. So then the next obvious question is: Why the heck not?”

How DNA Gains Lead to Losses

Feschotte’s best guess points at transposons themselves. “They provide a very natural mechanism by which gain provides the template to facilitate loss,” he said. Here’s how: As transposons multiply, they create long strings of nearly identical code. Parts of the genome become like a book that repeats the same few words. If you rip out a page, you might glue it back in the wrong place because everything looks pretty much the same. You might even decide the book reads just fine as is and toss the page in the trash. This happens with DNA too. When it’s broken and rejoined, as routinely happens when DNA is damaged but also during the recombination of genes in sexual reproduction, large numbers of transposons make it easy for strands to misalign, and that slippage can result in deletions. “The whole array can collapse at once,” Feschotte said.

Cedric Feschotte, a professor of molecular biology and genetics at Cornell University, recently of the University of Utah. University of Utah Health

This hypothesis hasn’t been tested in animals, but there is evidence from other organisms. “It’s not so different from what we’re seeing in plants with small genomes,” Leitch said. “DNA in these species is often dominated by just one or two types of transposons that amplify and then get eliminated. The turnover is very dynamic: in 3 to 5 million years, half of any new repeats will be gone.”

That’s not the case for larger genomes. “What we see in big plant genomes—and also in salamanders and lungfish—is a much more heterogeneous set of repeats, none of which are present in [large numbers],” Leitch said. She thinks these genomes must have replaced the ability to knock out transposons with a novel and effective way of silencing them. “What they do is, they stick labels onto the DNA that signal to it to become very tightly condensed—sort of squished—so it can’t be read easily.” That alteration stops the repeats from copying themselves, but it also breaks the mechanism for eliminating them. So over time, Leitch explained, “any new repeats get stuck and then slowly diverge through normal mutation to produce a genome full of ancient degenerative repeats.”