Remember that part in Casino Royale when Bond sips his martini, realizes he has been poisoned, then rushes out to his Aston Martin to inject himself with the antidote that Q thoughtfully stashed beforehand? This is exactly like that. Except, instead of Daniel Craig (*sigh*), it’s with worm larvae.

The roundworm Caenorhabditis elegans is a favorite laboratory model organism of geneticists and developmental biologists, mainly because it is simple, transparent, and easy to grow in bulk. Most worm researchers use the standard N2 strain, typically called the Bristol strain because it was isolated from mushroom compost in Bristol, England, in 1951.

Having a common reference strain like this is undoubtedly useful for labs spread across the world. But, like all species, C. elegans harbors genetic variability. Studies of wild strains can yield insights that would be missed if we assumed that N2 represented the entirety of worm genetics.

pha-1 is an essential gene in the N2 reference strain. N2 worms that have mutant pha-1 have pharyngeal defects (hence its name), so the gene was thought to be required for the development of the pharynx, which C. elegans use to eat. The lethality that results from a lack of pha-1 can be suppressed by mutations in another gene, sup-35; if sup-35 is inactivated, it doesn’t matter if pha-1 is inactivated, too. And, sup-35 over-expression mimics a loss of pha-1. The two genes obviously counteract each other.

When researchers looked at the genomes of wild worms from Hawaii, they noticed that they don’t have pha-1. So, clearly, the gene cannot be essential for worm development. When they crossed males from this wild strain with hermaphrodites that were N2 (that’s just how it works in these worms), half of the offspring died as embryos. This didn’t happen when the cross was done the other way around—N2 males and Hawaiian hermaphrodites. There was no lethality.

The antidote

This pattern is consistent with the N2 mother bestowing a toxin on all of her offspring, and only those offspring that produce an antidote survive. The gene for the antidote is found in the N2 genome but not in the genome from the wild strain, which is why half of the progeny die in some crosses. A lot of other genetic evidence, from this work as well as previous studies in other labs, bolstered this idea.

It turns out that pha-1’s essential function in the N2 genetic background is not in pharynx formation. Rather, pha-1 is necessary to act as an antidote to the toxin made by N2 moms and encoded by the sup-35 gene. That’s why N2 worms with nonfunctional pha-1 develop OK if sup-35 is not around. Since this genetic interaction had only been studied in the standard laboratory strain, its nature had been completely misinterpreted.

Selfish genetic elements like this sup-35/pha-1 dyad “subvert the laws of Mendelian segregation to promote their own transmission,” writes Ben-David. “Selfish elements can kill individuals that do not inherit them.” In addition to being crazy cool, this might have practical implications: since these elements will spread really well through populations, maybe we could hijack them to alter pathogen vectors, like mosquitoes, in the wild.

Of course, we may want to take our time with that, given we don’t yet really have a handle on how they work. One thing we do know, though: in worms at least, it is not only the mom that can lethally poison the brood. Ben-David’s lab previously identified another selfish genetic element, and this one had a sperm-delivered toxin.

Science, 2017. DOI: 10.1126/science.aan0621 (About DOIs).