Free Tasty by John McQuaid Page A

tenth of a second later, in perception, awareness: Ah, sweet. Ugh, bitter .
    The gene responsible for creating a bitter receptor was discovered, perhaps appropriately, not in a lab but in a computer database. By 1999, the first taste genes and receptors for sweetness, and closely related umami, had recently been isolated, and the scientists responsible had turned their attention to bitterness, performing experiments to isolate receptor cells. Meanwhile, they searched databases of the human genome, which had recently been decoded and published. Alot of it was still indecipherable strings of As, Cs, Gs, and Ts, the initials for DNA’s amino acids. One day, Ken Mueller, a graduate student at a Columbia taste lab, was poring over that hash of letters when he noticed that some strings of code looked awfully like those for the genes of already known receptors: a bit like rhodopsin, which detects light, with a dash of pheromone receptor. It turned out to be code for a bitter receptor. They dubbed it T2R1. Within months, they found sixteen more. The current count is about twenty-three, give or take.
    This mother lode explained a lot. There are only three genes for sweet taste, but the sweet receptor’s task is simple: find sugars. Nature is filled with so many poisons that a whole repertoire of bitter receptors is needed to detect them. Over hundreds of millions of years, gene replications (like the kind that gave jawless fish and other creatures ever-more-­powerful senses) doubled and quadrupled the array of bitter genes; natural selection tailored each of them to find different kinds of bitter. This is why only a few sugars taste sweet, while the number of bitter-tasting things is uncountable.
    T2R1 (now called TAS2R38) turned out to be Arthur Fox’s bitter gene. It’s a strand of DNA found on chromosome number seven. Small variations in this sequence alter the receptor’s chemical makeup and shape, creating the vast differences in people’s ability to taste PTC and overall bitter sensitivity.
    â€¢Â â€¢Â â€¢
    Isolating the DNA was, in some sense, the easy part. It was still not clear why nature programmed people with such diverse tastes—why some members of the Bush family loved broccoli while others despised it. There were deeper mysteriesbehind the bitter gene. Pursuing them inevitably led scientists back to where it all started: Africa.
    At the height of Fox’s taste-testing craze in the 1930s, a trio of English scientists became the first to explore the origins of the bitter gene. E. B. Ford, R. A. Fisher, and Julian Huxley were attending the annual International Congress of Genetics in Edinburgh in 1939 when they decided to do a PTC test on man’s closest relative, the chimpanzee. They tracked down a Glasgow scientist with a supply of the powder, mixed it into varying concentrations, bottled it up, and set off for the Edinburgh Zoo.
    They gave a medicine dropper full of bitter solution to one chimp. She spat it on Fisher. Another, enraged, tried to grab him. Bitter tasters, obviously. Six of the eight chimps were tasters and two were non-tasters, just how a random group of European humans might test. The zoo’s orangutans, gorillas, and gibbons had a similar mix. This work was later cut short by World War II, but its implication was fascinating: at some point before humans and chimps diverged millions of years ago, natural selection sorted primordial ape populations into groups of bitter tasters and non-tasters. Whatever advantages these paired traits conferred must have been powerful, because both had persisted for so long.
    It was a compelling theory. But once the bitter gene was decoded, it turned out to be dead wrong.
    Biologist Stephen Wooding revisited the question in the early 2000s using modern genetic tools. It had recently become possible to track the course of evolution by studying an animal’s genome. Over the eons, DNA mutates at a constant rate. Knowing