Read: What is a superbug?

Merrikh didn’t set out to beat antibiotic resistance. Originally, she didn’t even know she would be a scientist. She and her family fled from Iran when she was 3, settling in Turkey to avoid the war with Iraq. At 16, at her parents’ insistence, she moved to Texas to find an education. Stuck in an unfamiliar country with neither family nor money, she worked several poorly paid jobs to pay her way into college. Once there, she found her calling in biochemistry. Within 16 years, she was running her own lab.

At first, she studied the inner lives of bacteria, and the ways in which they copy their DNA and switch on their genes. That work bore unexpected fruit in 2015, when her team showed that a bacterial protein called Mfd can increase the rate at which genes mutate—that is, change their DNA. It was an unusual discovery. Other researchers had billed Mfd as a DNA-repairing protein, which would prevent mutations rather than promote them. But the more Merrikh studied Mfd, the less sense that made. For example, when her colleague Mark Ragheb removed it from bacteria, the microbes’ mutation rates fell by 50 to 80 percent.

That’s a big deal. Mutations are the fuel for evolution. If enough bacteria accumulate enough changes to enough genes, chances are that one of them will randomly acquire the ability to shrug off an antibiotic. So, in theory, if you can reduce mutation rates, you should also be able to delay the rise of resistance. The team proved this by exposing strains of Salmonella, with and without Mfd, to a battery of common antibiotics. After several generations, it found that strains that still had Mfd were between 6 and 21 times more resistant to the drugs than those without the protein.

The team repeated the experiment with other species of bacteria, and got results that were either similar or even more striking. For example, when it tested the bacterium behind tuberculosis, it found that Mfd-carrying strains became up to 1,000 times more resistant to antibiotics than the Mfd-less ones. “It applied to every bug we looked at and every antibiotic we tested,” Merrikh says. “The global nature of the effect is the most striking thing.”

That the loss of Mfd should be so universally debilitating makes sense because the protein itself is almost identical in a wide range of microbes, even distantly related ones. Usually, different bacteria will have their own takes on commonly shared proteins, like people speaking distinct dialects of a common language. But when it comes to Mfd, all bacteria essentially speak in the same accent. “Clearly this thing has a really important role,” Merrikh says.

Tami Lieberman from MIT says this approach has uses beyond stymieing superbugs. Many scientists are trying to genetically modify bacteria for industrial purposes, to pump out medicines or fuels. But those engineered microbes can evolve into obsolescence by picking up mutations that inactivate the foreign genes within them. “A synthetic biologist might consider deleting Mfd in their engineered strains to prolong their utility,” Lieberman says.