Here’s a question that occurs only to madmen and geneticists: How do you get a gene that kills an organism to spread through a whole population of that organism?
You can either make your gene deadly, and thus impossible to pass on, or not, and thus useless as a vector of attack. The solution has long been to try “silent” genes that can spread with no negative effects, either introducing a deadly weakness to a man-made chemical we withhold for a while, or by waiting for deadly activation by such a chemical. But recently, with the advent of advanced new in vivo gene editing technology, it’s become possible to make genes that seem to defy evolution — and that means we could soon start releasing animals carrying doomsday genes that spread with astonishing speed, quickly killing entire populations.
Such an animal is currently sitting in a laboratory at Imperial College London, an apocalypse mosquito carrying a gene that could one day end its entire species. It represents a controversial proposal to end the scourge of malaria, which kills hundreds of thousands of people each and every year, by wiping out the mosquitoes that spread the disease. It also represents a fundamentally new ability for humanity: the power to easily and selectively snuff out a subcategory of life on Earth. The name for this power is called gene drive.
Gene drive is simply the use of some strategy to artificially increase a gene’s inheritance rate. Such strategies are found all over nature, but despite decades of theorizing, nobody had a really viable way for mankind to harness this functionality through biotechnology. That’s changed thanks to the incredible advances in direct gene editing we’ve seen over the past half-decade, in particular the CRISPR/Cas9 gene editing suite.
These “molecular scissors” are actually borrowed from viruses, allowing scientists to swap out a gene in a living organism for one of their choice, edit it right into the genome so it will be passed on as the cells reproduce. If you can get your gene spliced into the “germ cells,” the pre-sperm or -egg cells of these organisms, then you can even introduce a chance that it will be passed on to the next generation — classically, without gene drive, you can introduce a 50% chance.
The chance is 50% because germ cells, like virtually all other cell types in humans and mosquitoes, have two copies of our genome. When we splice in our attack gene, it will end up sitting across from a second, totally normal copy of the gene it just replaced. This means that when the two copies get pulled apart to form the half-genomes of two new, separate sperm cells, only one of those new sperm cells will have our spliced-in sequence. The other will carry the same gene it would have, regardless.
So, if our spliced-in gene lowers evolutionary fitness, then all that will happen is the other half of the offspring will thrive, and the infected individuals will be quickly bred out of the population. And even if it’s a seemingly harmless silent gene that does nothing at first, it will still spread too slowly to change the overall population much at all.
Our mosquito doomsday device gets around these problems by applying two innovations.
Centenarians show successful aging as they remain active and alert at very old ages. Scientists at Stanford University and the University of Bologna have begun to unravel the basis for longevity by finding genetic loci associated with extreme longevity.
Previous work indicated that centenarians have health and diet habits similar to the average person, suggesting that factors in their genetic make-up could contribute to successful aging. However, prior genetic studies have identified only a single gene (APOE, known to be involved in Alzheimer’s disease) that was different in centenarians versus normal agers. The results from the current study indicate that several disease variants may be absent in centenarians versus the general population.