Pest populations of black rats and other rodents might eventually be eradicated with gene drives Nature Picture Library / Alamy Stock Photo

When it comes to mammals, both the optimism and the fears about gene drives are overblown. So say a team who have tested the concept in mice for the first time.

Their studies in mice suggests that existing gene drives don’t work nearly well enough to be used to eliminate mammalian pests – invasive rodents on islands, for instance. On the flip side, this means that gene drives would pose little danger to, say, wild mice if one somehow got out of a lab.

“I think we were all a little surprised because it works so well in insects,” says Kimberly Cooper of the University of California San Diego.


The gene drive concept emerged about 15 years ago. Most animals have two copies of the genome, but pass on only one copy to their offspring. The other parent contributes the second copy. This means there’s only a 50 per cent chance that any one offspring will inherit a specific piece of DNA from one parent.

Extinction drive

Gene drives are pieces of DNA that cheat. They “copy and paste” themselves from one genome copy to a target sequence in the other copy. In theory, that means there’s a 100 per cent chance that all offspring will inherit the gene drive and that it will spread through a population in relatively few generations.

In principle, then, a gene drive that made, say, all offspring male could quickly drive a species to extinction. In practice, the copying process does not always work. In addition, animals can become resistant if mutations appear in the genome region the “paste” process targets, which can prevent copying altogether.

Cooper found that in mice the copying process worked only 70 per cent of the time at best. What’s more, when the copying process failed it induced mutations in the target sequence, meaning that resistance to the gene drive could evolve very quickly and halt the spread of the drive.

Resistance is inevitable

A press release about the study hails these results as “Successful gene drive developed in lab mice”. Yet what Cooper tested was not a self-replicating gene drive but the separated components of a drive. This was done both for safety and convenience.

So it’s neither a gene drive nor successful in the sense of potentially providing a practical method for controlling mammalian pests. But it’s early days still and researchers could well find ways to dramatically improve the copying efficiency in mammals and to prevent resistance developing. “We would need to improve both,” says Cooper.

Meanwhile, the work does have potential benefits. The approach Cooper and her colleagues developed could provide a big boost to efforts to understand the causes of disease.

Researchers trying to work out what effect gene variants have on health often to need combine different traits in a single strain of animals. At present this can be prohibitively expensive, because as the number of traits to be combined goes up, says Cooper, the number of mice that have to be created via cross-breeding rises exponentially.

Using the gene drive concept – or “active genetics” as some call it – could change the odds and make this far more affordable.

Other groups have developed successful gene drives that might one day be used to eliminate the mosquitoes that carry malaria. Last year a team led by Andrea Crisanti of Imperial College London wiped out mosquito populations in small cages in a lab using a gene drive. The team will now carry out tests in much bigger cages in Italy designed to mimic conditions in the tropics.

Journal reference: Nature, DOI: 10.1038/s41586-019-0875-2