What if there was a humane, targeted way to wipe out alien pest species such as mice, rats and rabbits, by turning their own genes on themselves so they can no longer reproduce and their population collapses?
Gene drives – a technique that involves deliberately spreading a faulty gene throughout a population – promises to do exactly that.
Hype surrounding the technique continues to build, despite serious biosecurity, regulatory and ethical questions surrounding this emerging technology.
Our study, published today in the journal Proceedings of the Royal Society B, suggests that under certain circumstances, genome editing could work.
Good and bad genes
The simplest way to construct a gene drive aimed at suppressing a pest population is to identify a gene that is essential for the pest species’ reproduction or embryonic development. A new DNA sequence – the gene-drive “cassette” – is then inserted into that gene to disrupt its function, creating a faulty version (or “allele”) of that gene.
Typically, faulty alleles would not spread through populations, because the evolutionary fitness of individuals carrying them is reduced, meaning they will be less likely than non-faulty alleles to be passed on to the next generation. But the newly developed CRISPR gene-editing technology can cheat natural selection by creating gene-drive sequences that are much more likely to be passed on to the next generation.
Here’s how the trick works. The gene-drive cassette contains the genetic information to make two new products: an enzyme that cuts DNA, and a molecule called a guide RNA. These products act together as a tiny pair of molecular scissors that cuts the second (normal) copy of the target gene.
To fix the cut, the cell uses the gene drive sequence as a repair template. This results in a copy of the gene drive (and therefore the faulty gene) on both chromosomes.
This process is called “homing” and, when switched on in the egg- or sperm-producing cells of an animal, it should guarantee that almost all of their offspring inherit the gene-drive sequence.
As the gene-drive sequence spreads, mating between carriers becomes more likely, producing offspring that possess two faulty alleles and are therefore sterile or fail to develop past the embryonic stage.