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The Odin, in Oakland, California, is a company that sells genetic-engineering kits. The company’s founder, Josiah Zayner, has a shock of dyed-blond hair, multiple piercings, and a tattoo that urges: Create Something Beautiful. He holds a PhD in biophysics and is a well-known provocateur. Among his many stunts, he has coaxed his skin to produce a fluorescent protein, ingested a friend’s poop in a DIY fecal-matter transplant, and attempted to deactivate one of his genes so he could grow bigger biceps. (This last effort, he acknowledges, failed.) Zayner calls himself a “genetic designer” and has said his goal is to give people access to the resources they need to modify life in their spare time.
The Odin’s offerings range from a “Biohack the Planet” shot glass, which costs three bucks, to a “genetic engineering home lab kit,” which runs $1,849 and includes a centrifuge, a polymerase chain-reaction machine, and an electrophoresis gel box. I opted for something in between: the “bacterial CRISPR and fluorescent yeast combo kit,” which set me back $209. It came in a cardboard box decorated with the company’s logo, a twisting tree circled by a double helix. The tree, I believe, is supposed to represent Yggdrasil, whose trunk, in Norse mythology, rises through the center of the cosmos.
Inside the box, I found an assortment of lab tools—pipette tips, petri dishes, disposable gloves—as well as several vials containing E. coli and all I’d need to rearrange its genome. The E. coli went into the fridge, next to the butter. The other vials went into a bin in the freezer with the ice cream.
Genetic engineering is, by now, middle-aged. The first genetically engineered bacterium was produced in 1973. This was soon followed by a genetically engineered mouse, in 1974, and a genetically engineered tobacco plant, in 1983. The first genetically engineered food approved for human consumption, the Flavr Savr tomato, was licensed in 1994; it proved such a disappointment it went out of production a few years later. Genetically engineered varieties of corn and soy were developed at around the same time; these, in contrast to the Flavr Savr, have, in the United States, become more or less ubiquitous.
In the last decade or so, genetic engineering has undergone its own transformation, thanks to CRISPR. CRISPR is shorthand for a suite of techniques—most of them borrowed from bacteria—that make it vastly easier for researchers and biohackers to manipulate DNA. (The acronym stands for “clustered regularly interspaced short palindromic repeats.”) CRISPR allows its users to snip a stretch of DNA and then either disable the affected sequence or replace it with a new one.
The possibilities that follow are pretty much endless. Jennifer Doudna, a professor at the University of California, Berkeley and one of the developers of CRISPR, has put it like this: we now have “a way to rewrite the very molecules of life any way we wish.” With CRISPR, biologists have already created, among many, many other living things: ants that can’t smell, beagles that grow superhero-like muscles, pigs that resist swine fever, macaques that suffer from sleep disorders, coffee beans that contain no caffeine, salmon that don’t lay eggs, mice that don’t get fat, and bacteria whose genes contain, in code, Eadweard Muybridge’s famous series of photographs showing a racehorse in motion. A few years ago, a Chinese scientist, He Jiankui, announced that he had produced the world’s first CRISPR-edited humans—twin baby girls. According to He, the girls’ genes had been tweaked to confer resistance to HIV, though whether this is actually the case remains unclear. Shortly after he made the announcement, He was placed under house arrest in Shenzhen.
I have almost no experience in genetics and have not done hands-on lab work since high school. Nevertheless, by following the instructions that came in the box from The Odin, I was able, over the course of a weekend, to create a novel organism. First I grew up a colony of E. coli in one of the petri dishes. Then I doused it with the various proteins and bits of designer DNA I’d stored in the freezer. The process swapped out one “letter” of the bacteria’s genome, replacing an A (adenine) with a C (cytosine). Thanks to this emendation, my new and improved E. coli could, in effect, thumb its nose at streptomycin, a powerful antibiotic. If it felt a little creepy engineering a drug-resistant strain of E. coli in my kitchen, there was also a definite sense of achievement. So much so, in fact, that I decided to move on to the second project in the kit: inserting a jellyfish gene into yeast in order to make it glow.
The Australian Animal Health Laboratory, in the city of Geelong, is one of the most advanced high-containment laboratories in the world. It sits behind two sets of gates, the second of which is intended to foil truck bombers, and its poured-concrete walls are thick enough, I was told, to withstand a plane crash. There are five hundred and twenty air-lock doors at the facility and four levels of security. “It’s where you’d want to be in the zombie apocalypse,” a staff member told me. At the highest security level—Biosafety Level 4—are vials of some of the nastiest animal-borne pathogens on the planet, including Ebola. (The laboratory gets a shout-out in the movie Contagion.) Staff members who work in BSL-4 units can’t wear their own clothes into the lab and have to shower for at least three minutes before heading home. For their part, the animals at the facility can’t leave at all. “Their only way out is through the incinerator,” is how one employee put it to me.
Geelong is about an hour southwest of Melbourne. On the same trip that I met with Van Oppen, I paid a visit to the laboratory, which goes by the acronym AAHL (rhymes with “maul”). I’d heard about a gene-editing experiment going on there that intrigued me. As a result of yet another biocontrol effort gone awry, Australia is besieged by a species of giant toad known familiarly as the cane toad. In keeping with the recursive logic of the Anthropocene, researchers at AAHL were hoping to address this disaster with a further round of biocontrol. The plan involved editing the toad’s genome using CRISPR.
A biochemist named Mark Tizard, who was in charge of the project, had agreed to show me around. Tizard is a slight man with a fringe of white hair and twinkling blue eyes. Like many of the scientists I met in Australia, he’s from somewhere else, in his case London.
Before getting into amphibians, Tizard worked mostly on poultry. Several years ago, he and some colleagues at AAHL inserted a jellyfish gene into a hen. This gene, similar to the one I was planning to plug into my yeast, encodes a fluorescent protein. A chicken in possession of it will, as a consequence, give off an eerie glow under UV light. Next, Tizard figured out a way to insert the fluorescence gene so that it would be passed down to male offspring only. The result is a hen whose chicks can be sexed while they’re still in their shells.
Tizard knows that a lot of people are freaked out by genetically modified organisms. They find the idea of eating them repugnant and of releasing them into the world anathema. Though he’s no provocateur, he believes, like Zayner, that such people are looking at things all wrong.
“We have chickens that glow green,” Tizard told me. “And so we have school groups that come, and when they see the green chicken, you know, some of the kids go, ‘Oh, that’s really cool. Hey, if I eat that chicken, will I turn green?’ And I’m, like, ‘You eat chicken already, right? Have you grown feathers and a beak?’ ”
Anyway, according to Tizard, it’s too late in the day to be worried about a few genes here and there. “If you look at a native Australian environment, you see eucalyptus trees, koalas, kookaburras, whatever,” he said. “If I look at it, as a scientist, what I’m seeing is multiple copies of the eucalyptus genome, multiple copies of the koala genome, and so on. And these genomes are interacting with each other. Then, all of a sudden, ploomph, you put an additional genome in there—the cane toad genome. It was never there before, and its interaction with all these other genomes is catastrophic. It takes other genomes out completely.
“What people are not seeing is that this is already a genetically modified environment,” he went on. Invasive species alter the environment by adding entire genomes that don’t belong. Genetic engineers, by contrast, alter just a few bits of DNA here and there.
“What we’re doing is potentially adding on maybe ten more genes onto the twenty thousand toad genes that shouldn’t be there in the first place, and those ten will sabotage the rest and take them out of the system and so restore balance,” Tizard said. “The classic thing people say with molecular biology is: Are you playing God? Well, no. We are using our understanding of biological processes to see if we can benefit a system that is in trauma.”
Formally known as Rhinella marina, cane toads are a splotchy brown, with thick limbs and bumpy skin. Descriptions inevitably emphasize their size. “Rhinella marina is an enormous, warty bufonid (true toad),” notes the U.S. Fish and Wildlife Service. “Large individuals sitting on roadways are easily mistaken for boulders,” observes the U.S. Geological Survey. The biggest cane toad ever recorded was fifteen inches long and weighed almost six pounds—as much as a chubby chihuahua. A toad named Bette Davis, who lived at the Queensland Museum, in Brisbane, in the 1980s, was nine and a half inches long and almost as wide—about the size of a dinner plate. The toads will eat almost anything they can fit in their oversized mouths, including mice, dog food, and other cane toads.
Cane toads are native to South America, Central America, and the very southernmost tip of Texas. In the mid-1800s, they were imported to the Caribbean. The idea was to enlist the toads in the battle against beetle grubs, which were plaguing the region’s cash crop—sugar cane. (Sugar cane, too, is an imported species; it is native to New Guinea.) From the Caribbean, the toads were shipped to Hawaii and from there, to Australia. In 1935, a hundred and two toads were loaded onto a steamer in Honolulu. A hundred and one of them survived the journey and ended up at a research station in sugar-cane country, on Australia’s northeast coast. Within a year, they’d produced more than 1.5 million eggs. The resulting toadlets were intentionally released into the region’s rivers and ponds.
It’s doubtful that the toads ever did the sugar cane much good. Cane grubs perch too high off the ground for a boulder-sized amphibian to reach. This didn’t faze the toads. They found plenty else to eat and continued to produce toadlets by the truckload. From a sliver of the Queensland coast, they pushed north, into the Cape York Peninsula, and south, into New South Wales. Sometime in the 1980s, they crossed into the Northern Territory. In 2005, they reached a spot known as Middle Point, in the western part of the Territory, not far from the city of Darwin.
Along the way, something curious happened. In the early phase of the invasion, the toads were advancing at the rate of about six miles a year. A few decades later, they were moving at twelve miles a year. By the time they hit Middle Point, they’d sped up to thirty miles a year. When researchers measured the toads at the invasion front, they found out why. The toads on the front lines had significantly longer legs than the toads back in Queensland. And this trait was heritable. The Northern Territory News played the story on its front page, under the headline Super Toad. Accompanying the article was a doctored photo of a cane toad wearing a cape. “It has invaded the Territory and now the hated cane toad is evolving,” the newspaper gasped. Contra Darwin, it seemed, evolution could be observed in real time.
Cane toads are not just disturbingly large; from a human perspective, they’re also ugly, with bony heads and what looks like a leering expression. The trait that makes them truly “hated,” though, is that they’re toxic. When an adult is bitten or feels threatened, it releases a milky goo that swims with heart-stopping compounds. Dogs often suffer cane toad poisoning, the symptoms of which range from frothing at the mouth to cardiac arrest. People who are foolish enough to consume cane toads usually wind up dead.
Australia has no poisonous toads of its own; indeed, it has no toads at all. So its native fauna hasn’t evolved to be wary of them. The cane toad story is thus the Asian carp story inside out, or maybe upside down. While carp are a problem in the United States because nothing eats them, cane toads are a menace in Australia because just about everything eats them. The list of species whose numbers have crashed due to cane toad consumption is long and varied. It includes: freshwater crocodiles, which Australians call “freshies”; yellow-spotted monitor lizards, which can grow up to five feet long; northern blue-tongued lizards, which are actually skinks; water dragons, which look like small dinosaurs; common death adders, which, as the name suggests, are venomous snakes; and king brown snakes, which are also venomous. By far the most winning animal on the victims list is the northern quoll, a sweet-looking marsupial. Northern quolls are about a foot long, with pointy faces and spotted brown coats. When young quolls graduate from their mother’s pouch, she carries them around on her back.
In an effort to slow down the cane toads, Australians have come up with all sorts of ingenious and not-so-ingenious schemes. The Toadinator is a trap fitted out with a portable speaker that plays the cane toad’s song, which some compare to a dial tone and others to the thrum of a motor. Researchers at the University of Queensland have developed a bait that can be used to lure cane toad tadpoles to their doom. People shoot cane toads with air rifles, whack them with hammers, bash them with golf clubs, purposefully run them over with their cars, stick them in the freezer until they solidify, and spray them with a compound called HopStop, which, buyers are assured, “anesthetizes toads within seconds” and dispatches them within an hour. Communities organize “toad busting” militias. A group called the Kimberley Toad Busters has recommended that the Australian government offer a bounty for each toad eliminated. The group’s motto is: “If everyone was a toad buster the toads would be busted!”
At the point Tizard got interested in cane toads, he’d never actually seen one. Geelong lies in a region—southern Victoria—the toads haven’t yet conquered. But one day at a meeting, he was seated next to a molecular biologist who studied the amphibian. She told him that, despite all the busting, the toads kept on spreading.
“She said, it was such a shame, if only there was some new way of getting at it,” Tizard recalled. “Well, I sat down and scratched my head.
“I thought: Toxins are generated by metabolic pathways,” he went on. “That means enzymes, and enzymes have to have genes to encode them. Well, we have tools that can break genes. Maybe we can break the gene that leads to the toxin.”
Tizard brought on a post-doc named Caitlin Cooper to help with the mechanics. Cooper has shoulder-length brown hair and an infectious laugh. (She, too, is from somewhere else—in her case Massachusetts.) No one had ever tried to gene edit a cane toad before, so it was up to Cooper to figure out how to do it. Cane toad eggs, she discovered, had to be washed and then pierced just so, with a very fine pipette, and this had to be done quickly, before they had time to start dividing. “Refining the micro-injection technique took quite a while,” she told me.
As sort of a warm-up exercise, Cooper set out to change the cane toad’s color. A key pigment gene for toads (and, for that matter, humans) codes for the enzyme tyrosinase, which controls the production of melanin. Disabling this pigment gene should, Cooper reasoned, produce toads that were light-colored instead of dark. She mixed some eggs and sperm in a petri dish, micro-injected the resulting embryos with various CRISPR-related compounds, and waited. Three oddly mottled tadpoles emerged. One of the tadpoles died. The other two—both males—grew into mottled toadlets. They were christened Spot and Blondie. “I was absolutely rapt when this happened,” Tizard told me.
Cooper next turned her attention to “breaking” the toads’ toxicity. Cane toads store their poison in glands behind their shoulders. In its raw form, this poison is merely sickening. But toads can, when attacked, produce an enzyme—bufotoxin hydrolase—that amplifies the poison’s potency a hundredfold. Using CRISPR, Cooper edited a second batch of embryos to delete a section of the gene that codes for bufotoxin hydrolase. The result was a batch of detoxified toadlets.
After we’d talked for a while, Cooper offered to show me her toads. This entailed penetrating deeper into AAHL, through more air-lock doors and layers of security. We all put scrubs on over our clothes and booties over our shoes. Cooper spritzed my tape recorder with some kind of cleaning fluid. Quarantine Area, a sign said. Heavy Penalties Apply. I decided it would be better not to mention The Odin and my own rather less secure gene-editing adventures.
Beyond the doors was a sort of antiseptic barnyard, filled with animals in various sized enclosures. The smell was a cross between hospital and petting zoo. Near a block of mouse cages, the detox toadlets were hopping around a plastic tank. There were a dozen of them, about ten weeks old and each about three inches long.
“They’re very lively, as you can see,” Cooper said. The tank had been outfitted with everything a person could imagine a toad would want—fake plants, a tub of water, a sunlamp. I thought of Toad Hall, “replete with every modern convenience.” One of the toads stuck out its tongue and nabbed a cricket.
“They will eat literally anything,” Tizard said. “They’ll eat each other. If a big one encounters a small one, it’s lunch.”
Let loose in the Australian countryside, a knot of detox toads presumably wouldn’t last long. Some would become lunch, either for freshies or lizards or death adders, and the rest would be outbred by the hundreds of millions of toxic toads already hopping across the landscape.
What Tizard had in mind for them was a career in education. Research on quolls suggests that the marsupials can be trained to steer clear of cane toads. Feed them toad “sausages” laced with an emetic, and they will associate toads with nausea and learn to avoid them. Detox toads, according to Tizard, would make an even better training tool: “If they’re eaten by a predator, the predator will get sick but not die, and it will go, ‘I’m never eating a toad again.’ ”
Before they could be used for teaching quolls—or for any other purpose—the detox toads would need a variety of government permits. When I visited, Cooper and Tizard hadn’t started in on the paperwork, but they were already contemplating other ways to tinker. Cooper thought it might be possible to fiddle with the genes that produce the gel coat on the toads’ eggs in such a way that the eggs would be impossible to fertilize.
“When she described the idea to me, I was, like, brilliant!” Tizard said. “If we can take steps to knock down their fecundity, that’s absolute gold.” (A female cane toad can produce up to thirty thousand eggs at a go.)
A few feet away from the detox toads, Spot and Blondie were sitting in their own tank, an even more elaborate affair, with a picture of a tropical scene propped in front for their enjoyment. They were almost a year old and now fully grown, with thick rolls of flesh around their midsections, like sumo wrestlers. Spot was mostly brown, with one yellowish hind leg; Blondie was more richly variegated, with whitish hind legs and light patches on his forelimbs and chest. Cooper reached a gloved hand into the tank and pulled out Blondie, whom she’d described to me as “beautiful.” He immediately peed on her. He appeared to be smiling malevolently, though I realized, of course, that wasn’t actually the case. He had, it seemed to me, a face only a genetic engineer could love.
According to the standard version of genetics that kids learn in school, inheritance is a roll of the dice. Let’s say a person (or a toad) has received one version of a gene from his mother—call it A—and a rival version of this gene—A1—from his father. Then any child of his will have even odds of inheriting an A or an A1, and so on. With each new generation, A and A1 will be passed down according to the laws of probability.
Like much else that’s taught in school, this account is only partly true. There are genes that play by the rules and there are also renegades that refuse to. Outlaw genes fix the game in their favor and do so in a variety of devious ways. Some interfere with the replication of a rival gene; others make extra copies of themselves, to increase their odds of being passed down; and still others manipulate the process of meiosis, by which eggs and sperm are formed. Such rule-breaking genes are said to “drive.” Even if they confer no fitness advantage—indeed, even if they impose a fitness cost—they’re handed on more than half of the time. Some particularly self-serving genes are passed on more than ninety percent of the time. Driving genes have been discovered lurking in a great many creatures, including mosquitoes, flour beetles, and lemmings, and it’s believed they could be found in a great many more, if anyone took the trouble to look for them. (It’s also true that the most successful driving genes are tough to detect, because they’ve driven other variants to oblivion.)
Since the 1960s, it’s been a dream of biologists to exploit the power of gene drives—to drive the drive, as it were. This dream has now been realized, and then some, thanks to CRISPR.
In bacteria, which might be said to hold the original patent on the technology, CRISPR functions as an immune system. Bacteria that possess a “CRISPR locus” can incorporate snippets of DNA from viruses into their own genomes. They use these snippets, like mug shots, to recognize potential assailants. Then they dispatch CRISPR-associated, or Cas, enzymes, which work like tiny knives. The enzymes slice the invaders’ DNA at critical locations, thus disabling them.
Genetic engineers have adapted the CRISPR-Cas system to cut pretty much any DNA sequence they wish. They’ve also figured out how to induce a damaged sequence to stitch into itself a thread of foreign DNA it’s been supplied with. (This is how my E. coli were fooled into replacing an adenine with a cytosine.) Since the CRISPR-Cas system is a biological construct, it, too, is encoded in DNA. This turns out to be key to creating a gene drive. Insert the CRISPR-Cas genes into an organism, and the organism can be programmed to perform the task of genetic reprogramming on itself.
In 2015, a group of scientists at Harvard announced they’d used this self-reflexive trick to create a synthetic gene drive in yeast. (Starting with some cream-colored yeast and some red yeast, they produced colonies that, after a few generations, were all red.) This was followed three months later by an announcement from researchers at UC–San Diego that they’d used much the same trick to create a synthetic gene drive in fruit flies. (Fruit flies are normally brown; the drive, pushing a gene for a kind of albinism, yielded offspring that were yellow.) And six months after that, a third group of scientists announced they had created a gene-drive Anopheles mosquito.
If CRISPR confers the power to “rewrite the very molecules of life,” with a synthetic gene drive, that power increases exponentially. Suppose that the researchers in San Diego had released their yellow fruit flies. Assuming those flies had found mates, swarming around some campus dumpster, their offspring, too, would have been yellow. And assuming those offspring survived and also successfully mated, their progeny would, in turn, have been yellow. The trait would have continued to spread, ineluctably, from the redwood forest to the Gulf Stream waters, until yellow ruled.
And there’s nothing special about color in fruit flies. Just about any gene in any plant or animal can—in principle, at least—be programmed to load the inheritance dice in its favor. This includes genes that have themselves been modified or borrowed from other species. It should be possible, for example, to engineer a drive that would spread a broken-toxin gene among cane toads. It may also be possible one day to create a drive for corals that would push a gene for heat tolerance.
In a world of synthetic gene drives, the border between the human and the natural, between the laboratory and the wild, already deeply blurred, all but dissolves. In such a world, not only do people determine the conditions under which evolution is taking place, people can—again, in principle—determine the outcome.
The first mammal to be fitted out with a CRISPR-assisted gene drive will, almost certainly, be a mouse. Mice are what’s known as a “model organism.” They breed quickly, are easy to raise, and their genome has been intensively studied.
Paul Thomas is a pioneer in mouse research. His lab is in Adelaide, at the South Australian Health and Medical Research Institute, a sinuous building covered in pointy metal plates. (Adelaideans refer to the building as the “cheese grater”; when I went to visit, I thought it looked more like an ankylosaurus.) As soon as a breakthrough paper on CRISPR was published, in 2012, Thomas recognized it as a game changer. “We jumped on it straightaway,” he told me. Within a year, his lab had used CRISPR to engineer a mouse afflicted with epilepsy.
When the first papers on synthetic gene drives came out, Thomas once again plunged in: “Being interested in CRISPR and being interested in mouse genetics, I couldn’t resist the opportunity to try to develop the technology.” Initially, his goal was just to see if he could get the technology to work. “We didn’t really have much funding,” he said. “We were doing it on the smell of an oily rag, and these experiments, they’re quite expensive.”
While Thomas was still, in his words, “just dabbling,” he was contacted by a group that calls itself GBIRd. The acronym (pronounced “gee-bird”) stands for Genetic Biocontrol of Invasive Rodents, and the group’s ethos might be described as Dr. Moreau joins Friends of the Earth.
“Like you, we want to preserve our world for generations to come,” GBIRd’s website says. “There is hope.” The site features a picture of an albatross chick gazing lovingly at its mother.
GBIRd wanted Thomas’s help designing a very particular kind of mouse drive—a so-called “suppression drive.” A suppression drive is designed to defeat natural selection entirely. Its purpose is to spread a trait so deleterious that it can wipe out a population. Researchers in Britain have already engineered a suppression drive for Anopheles gambiae mosquitoes, which carry malaria. Their goal is eventually to release such mosquitoes in Africa.
Thomas told me there were various ways to go about designing a self-suppressing mouse, most having to do with sex. He was particularly keen on the idea of an “X-shredder” mouse.
Mice, like other mammals, have two sex-determining chromosomes—XXs are female, XYs male. Mice sperm carry a single chromosome, either an X or a Y. An X-shredder mouse is a mouse who’s been gene edited so that all of his X-bearing sperm are defective.
“Half the sperm drop out of the sperm pool, if you like,” Thomas explained. “They can’t develop anymore. That leaves you with just Y-bearing sperm, so you get all male progeny.” Put the shredding instructions on the Y chromosome and the mouse’s offspring will, in turn, produce only sons, and so on. With each generation, the sex imbalance will grow, until there are no females left to reproduce.
Thomas explained that work on a gene-drive mouse was going slower than he’d hoped. Still, he thought by the end of the decade someone would develop one. It might be an X-shredder, or it might rely on a design that’s yet to be imagined. Mathematical modeling suggests that an effective suppression drive would be extremely efficient; a hundred gene-drive mice released on an island could take a population of fifty thousand ordinary mice down to zero within a few years.
“So that’s quite striking,” Thomas said. “It’s something to aim for.”
If the Anthropocene’s clearest geological marker is a spike in radioactive particles, its clearest biological marker may be a spike in rodents. Everywhere humans have settled on the planet—and even some places they’ve only visited—mice and rats have tagged along, often with ugly consequences.
The Pacific rat (Rattus exulans) was once confined to Southeast Asia. Starting about three thousand years ago, seafaring Polynesians carried it to nearly every island in the Pacific. Its arrival set off wave after wave of destruction that claimed at least a thousand species of island birds. Later, European colonists brought to those same islands—and to many others—ship rats (Rattus rattus), thus setting off further waves of extinctions, which are still ongoing. In the case of New Zealand’s Big South Cape Island, ship rats didn’t arrive until the 1960s, by which point naturalists were on hand to document the results. Despite intensive efforts to save them, three species endemic to the island—one bat and two birds—disappeared.
The house mouse (Mus musculus) originated on the Indian subcontinent; it can now be found from the tropics to very near the poles. According to Lee Silver, author of Mouse Genetics, “Only humans are as adaptable (some would say less so).” Under the right circumstances, mice can be just as fierce as rats, and every bit as deadly. Gough Island, which lies more or less midway between Africa and South America, is home to the world’s last two thousand pairs of Tristan albatrosses. Video cameras installed on the island have recorded gangs of Mus musculus attacking albatross chicks and eating them alive. “Working on Gough Island is like working in an ornithological trauma center,” Alex Bond, a British conservation biologist, has written.
For the last few decades, the weapon of choice against invasive rodents has been Brodifacoum, an anticoagulant that induces internal hemorrhaging. Brodifacoum can be incorporated into bait and then dispensed from feeders, or it can be spread by hand, or dropped from the air. (First you ship a species around the world, then you poison it from helicopters!) Hundreds of uninhabited islands have been de-moused and de-ratted in this way, and such campaigns have helped bring scores of species back from the edge, including New Zealand’s Campbell Island teal, a small, flightless duck, and the Antiguan racer, a grayish lizard-eating snake.
The downside of Brodifacoum, from a rodent’s perspective, is pretty obvious: internal bleeding is a slow and painful way to go. From an ecologist’s perspective, too, there are drawbacks. Non-target animals often take the bait or eat rodents that have eaten it. In this way, poison spreads up and down the food chain. And if just one pregnant mouse survives an application, she can repopulate an entire island.
Gene-drive mice would scuttle around these problems. Impacts would be targeted. There would be no more bleeding to death. And, perhaps best of all, gene-drive rodents could be released on inhabited islands, where dropping anticoagulants from the air is, understandably, frowned upon.
But as is so often the case, solving one set of problems introduces new ones. In this case, big ones. Humongous ones. Gene-drive technology has been compared to Kurt Vonnegut’s ice-nine, a single shard of which is enough to freeze all the water in the world. A single X-shredder mouse on the loose could, it’s feared, have a similarly chilling effect—a sort of mice-nine.
To guard against a Vonnegutian catastrophe, various fail-safe schemes have been proposed, with names like “killer-rescue,” “multi-locus assortment,” and “daisy-chain.” All of them share a basic, hopeful premise: that it should be possible to engineer a gene drive that’s effective and at the same time not too effective. Such a drive might be engineered so as to exhaust itself after a few generations, or it might be yoked to a gene variant that’s limited to a single population on a single island. It has also been suggested that if a gene drive did somehow manage to go rogue, it might be possible to send out into the world another gene drive, featuring a so-called CATCHA sequence, to chase it down. What could possibly go wrong?
While I was in Australia, I wanted to get out of the lab and into the countryside. I thought it would be fun to see some northern quolls; in the photos I’d found online, they looked awfully cute—a bit like miniature badgers. But when I asked around, I learned that quoll-spotting required a lot more expertise and time than I had. It would be much easier to find some of the amphibians that were killing them. So one evening I set out with a biologist named Lin Schwarzkopf to go toad hunting.
As it happened, Schwarzkopf was one of the inventors of the Toadinator trap, and we stopped by her office, at James Cook University, to take a look at the device. It was a cage about the size of a toaster oven, with a plastic-flap door. When Schwarzkopf turned on the trap’s little speaker, the office reverberated with the toad’s thrumming call.
“Male toads are attracted to anything that sounds even remotely like a cane toad,” she told me. “If they hear a generator, they’ll go to it.”
James Cook University is situated on the northern Queensland coast, in the region where the toads were first introduced. Schwarzkopf figured we should be able to locate some toads right on the university grounds. We both strapped on headlamps. It was about 9 p.m., and the campus was deserted, except for the two of us and a family of wallabies hopping about. We wandered around for a while, looking for the glint of a malevolent eye. Just as I was beginning to lose heart, Schwarzkopf spotted a toad in the leaf litter. Picking it up, she immediately identified it as a female.
“They won’t hurt you unless you give them a really hard time,” she said, pointing out the toad’s toxin glands, which looked like two baggy pouches. “That’s why you shouldn’t hit them with a golf club. Because if you hit the glands, the poison can spray out. And if it gets in your eyes, it will blind you for a few days.”
We wandered around some more. It had been so dry, Schwarzkopf observed, the toads were probably short on moisture: “They love air-conditioning units—anything that’s dripping.” Near an old greenhouse, where someone had recently run a hose, we found two more toads. Schwarzkopf flipped over a rotting crate the size and shape of a casket. “The mother lode!” she announced. In about a quarter-inch of scummy water were more cane toads than I could count. Some of the toads were sitting on top of one another. I thought they might try to get away; instead, they sat there, unperturbed.
The strongest argument for gene editing cane toads, house mice, and ship rats is also the simplest: what’s the alternative? Rejecting such technologies as unnatural isn’t going to bring nature back. The choice is not between what was and what is, but between what is and what will be, which, often enough, is nothing. This is the situation of the Devils Hole pupfish, the Shoshone pupfish, and the Pahrump poolfish, of the northern quoll, the Campbell Island teal, and the Tristan albatross. Stick to a strict interpretation of the natural and these—along with thousands of other species—are goners. The issue, at this point, is not whether we’re going to alter nature, but to what end?
“We are as gods and might as well get good at it,” Stewart Brand, editor of the Whole Earth Catalog, famously wrote in its first issue, published in 1968. Recently, in response to the whole-earth transformation that’s under way, Brand has sharpened his statement: “We are as gods and have to get good at it.” Brand has co-founded a group, Revive & Restore, whose stated mission is to “enhance biodiversity through new techniques of genetic rescue.” Among the more fantastic projects the group has backed is an effort to resurrect the passenger pigeon. The idea is to reverse history by rejiggering the genes of the bird’s closest living relative, the band-tailed pigeon.
Much closer to realization is an effort to bring back the American chestnut tree. The tree, once common in the eastern United States, was all but wiped out by chestnut blight. (The blight, a fungal pathogen introduced in the early twentieth century, killed off nearly every chestnut in North America—an estimated four billion trees.) Researchers at the SUNY College of Environmental Science and Forestry, in Syracuse, New York, have created a genetically modified chestnut that’s immune to blight. The key to this resistance is a gene imported from wheat. Owing to this single borrowed gene, the tree is considered transgenic and subject to federal permitting. As a consequence, the blight-resistant saplings are, for now, confined to greenhouses and fenced-in plots.
As Tizard points out, we’re constantly moving genes around the world, usually in the form of entire genomes. This is how chestnut blight arrived in North America in the first place; it was carried in on Asian chestnut trees, imported from Japan. If we can correct for our earlier tragic mistake by shifting just one more gene around, don’t we owe it to the American chestnut to do so? The ability to “rewrite the very molecules of life” places us, it could be argued, under an obligation.
Of course, the argument against such intervention is also compelling. The reasoning behind “genetic rescue” is the sort responsible for many a world-altering screwup. (See, for example, Asian carp and cane toads.) The history of biological interventions designed to correct for previous biological interventions reads like Dr. Seuss’s The Cat in the Hat Comes Back, in which the Cat, after eating cake in the bathtub, is asked to clean up after himself:
Do you know how he did it?
WITH MOTHER’S WHITE DRESS!
Now the tub was all clean,
But her dress was a mess!
In the 1950s, Hawaii’s Department of Agriculture decided to control giant African snails, which had been introduced two decades earlier as garden ornaments, by importing rosy wolfsnails, which are also known as cannibal snails. The cannibal snails mostly left the giant snails alone. Instead, they ate their way through dozens of species of Hawaii’s small endemic land snails, producing what E. O. Wilson has called “an extinction avalanche.”
Responding to Brand, Wilson has observed, “We are not as gods. We’re not yet sentient or intelligent enough to be much of anything.”
Paul Kingsnorth, a British writer and activist, has put it this way: “We are as gods, but we have failed to get good at it…We are Loki, killing the beautiful for fun. We are Saturn, devouring our children.”
Kingsnorth has also observed, “Sometimes doing nothing is better than doing something. Sometimes it is the other way around.”