In February of 1967, German biologist Hannes Laven hiked to a village 16 miles north of Yangon, Myanmar. He carried with him 100 mosquitoes from Fresno, California—50 males that had been infected with a bacteria called Wolbachia, and 50 females that had not. He bred these mosquitoes together, separated out the males from the thousands of offspring, and released them around the town’s 150 thatched-roof houses. Twelve weeks and six generations of California-Myanmar cross-breeding later he had eradicated the entire local mosquito population: None of their eggs would hatch.

For 50 years, scientists have known that Wolbachia can cause sterility in mosquitoes and other insects. But now, for the first time, they finally understand exactly how it works. That’s important, because right now the only large-scale solutions to mosquito-carried diseases like Zika, dengue fever, and malaria involve spraying huge amounts of pesticides. In two papers out today, in Nature and Nature Microbiology, researchers at Yale and Vanderbilt have finally cracked how the bacteria gives mosquitoes the snip-snip, making it possible to develop even better Wolbachia-based pesticides that could supplant the chemical standbys.

Wolbachia lives in the cells of lots of insects, but noticeably, not in Aedes aegypti, the mosquito species that carries Zika, dengue, and yellow fever. You’ll notice, though, that the billions of insects naturally infected with Wolbachia can breed just fine. That’s because the bacteria carries two genes that influence sterility—one that works like a toxin, the other like an antidote. Biochemist John Beckmann discovered the two genes in 2013, and spent the last four years figuring out exactly what they do. It took that long because it's one seriously complicated system.

Here's how his team thinks it works: The toxin gene makes a cutting enzyme that keeps the chromosomes in mosquito sperm from pulling apart when the embryo’s cells start dividing. The other gene, the rescue gene, makes a protein that binds to that enzyme, preventing it from messing with the sperm cells. Now, normally that rescue protein breaks down in sperm, so it doesn't do any good. But if the *Wolbachia-*infected male mates with a female infected with the same strain, her bacteria pump the antidote protein back into the embryo, rescuing its ability to divide. Voila: normal insect baby.

What this means is that for the sterilization technique to work in the wild, there can’t be any females in the area with a copy of that bacterial rescue gene. So to target mosquitoes, scientists use Wolbachia pretty much the way Hannes Leven did—rearing millions of sterile males and dumping them into the wild. They’ll outmate the fertile males in the area, produce only dead eggs, and drive the mosquito population down.

That’s exactly what entomologist Stephen Dobson has been doing in Clovis, California, just a few miles from where Leven’s mosquitoes came from. Last summer, Dobson’s company, MosquitoMate, released 500,000 Aedes aegypti mosquitoes into one of the town’s subdivisions—all male, all infected with a strain of Wolbachia—to attack the wild mosquito population.

Dobson says the experiment was a success—but it had its challenges. For one thing, the first few strains of Wolbachia the company tried didn’t work. The bacteria all cause inviable embryos in slightly different ways, so not all strains work for all insects. And making sure not to release any females is super work-intensive: An employee visually inspects each one before they get shipped out. If a female infected with the same strain of Wolbachia gets out, her eggs will be fertile, and they’ll pass on that bacterial antidote gene to their offspring too. “It can kill the whole program,” says Beckmann.

But using a transgenic approach, based on Beckmann’s discovery, solves those problems. Rather than removing the antidote gene by removing females from a population, you could instead edit the antidote gene out of Wolbachia, which eliminates the possibility that any eggs survive. Or you can put the sterility gene right into the mosquito, skipping Wolbachia entirely. That's what Beckmann's group did. And they found that transgenic females don't rescue the embryos; only Wolbachia does. “We can basically hack this system by engineering constructs that can’t be rescued,” he says, “which is way better than just the bacterial infection.”

Dobson admits that Beckmann’s work is a huge leap forward for the field. And will make it a lot easier to limit the amount of trial and error involved finding the right strain to infect his bugs. But the work also addresses the big white mosquito in the room—the GMO. Putting in a toxic gene, or taking out a rescue one, both involve genetic engineering. And that doesn’t always go over so well.

Last November, the residents of Key Haven, Florida voted down a trial of UK-based company Oxitec’s genetically engineered mosquitoes after local activists rallied the community. The company is currently reviewing alternative trial sites elsewhere in Florida with the Food and Drug Administration. But while they wait, MosquitoMate is moving in. Dobson is gearing up to start his own trial in the Florida Keys sometime this summer. And since he’s not using transgenic mosquitoes, he doesn’t have to go through the FDA either. Instead he’s been working with the Environmental Protection Agency to get a biopesticide designation—a much less burdensome process. He expects to get that designation, not for Aedes aegypti, but for a different mosquito he’s been testing since 2014, by the end of this year.

Beckmann isn’t expecting to convert everyone. And in fact, that would be counterproductive. Sterilization supercharges the effects of natural selection, putting huge pressure on females to sniff out males who still have all their goods. Nature is always going to select for traits that yield offspring, so it’s crucial to have multiple methods that scientists and mosquito management teams can switch between to prevent resistance. These new Wolbachia revelations should provide some options. But preventing public resistance to a genetically engineered answer to Zika? That’s someone else’s problem.