De-extinction could soon become reality – and the International Union for the Conservation of Nature is already making plans to encourage proper use of the technology.
Early on an unusually blustery day in June, Kevin Esvelt climbed aboard a ferry at Woods Hole, bound for Nantucket Island. Esvelt, an assistant professor of biological engineering at the Massachusetts Institute of Technology, was on his way to present to local health officials a plan for ridding the island of one of its most persistent problems: Lyme disease. He had been up for much of the night working on his slides, and the fatigue showed. He had misaligned the buttons on his gray pin-striped shirt, and the rings around his deep-blue eyes made him look like a sandy-haired raccoon.
Esvelt, who is thirty-four, directs the “sculpting evolution” group at M.I.T., where he and his colleagues are attempting to design molecular tools capable of fundamentally altering the natural world. If the residents of Nantucket agree, Esvelt intends to use those tools to rewrite the DNA of white-footed mice to make them immune to the bacteria that cause Lyme and other tick-borne diseases. He and his team would breed the mice in the laboratory and then, as an initial experiment, release them on an uninhabited island. If the number of infected ticks begins to plummet, he would seek permission to repeat the process on Nantucket and on nearby Martha’s Vineyard.
Gene editing involves altering or disabling existing genes, which used to be extremely difficult. It took many years to develop the gene-editing tool that saved Layla, but thanks to a revolutionary method known as CRISPR, this can now be done in just weeks.
In fact, CRISPR works so well that the first human trial involving the method has already begun. In China, it is being used to disable a gene called PD-1 in immune cells taken from individuals with cancer. The edited cells are then injected back into each person’s body. PD-1 codes for an “off switch” on the surface of immune cells, and many cancers evolve the ability to thwart immune attacks by flipping the PD-1 switch to “off”. On the edited immune cells there is no switch for cancer cells to flip.
North Dakota is not known for its pigeons. Or forests, for that matter. The state bird is the western meadowlark, a mellifluous yellow songbird often seen singing on fence posts. Such posts substitute for trees in much of North Dakota. The state is primarily covered in what was once short-grass prairie but is now mostly farms embedded in a human-made grassland, exceptions being the Badlands and a swath of boreal forest in the far north near Canada.
Yet it was near Williston, the heart of western North Dakota’s new boom-and-bust oil patch, that Ben Novak first fell in love with Ectopistes migratorius—the passenger pigeon, a bird that rarely graced this region, if ever.
UC Berkeley biochemist Jennifer Doudna, molecular biologist Robert Tijan and a team of researchers have expanded the role of the newly discovered CRISPR protein C2c2 that targets RNA instead of DNA.
C2c2 has been described as an RNA-guided RNA-cutting enzyme; however, a full understanding of how this protein acts to cleave RNA was lacking. In a paper published today in Nature titled “Two distinct RNase activities of CRISPR-C2c2 enable guide-RNA processing and RNA detection,” the researchers were able to show that C2c2 has not one, as previously thought, but two distinct RNA cutting activities that in concert can be harnessed for robust RNA detection and degradation.