Sun. Feb 5th, 2023

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Enlarge / C. eleganswith the pharynx at the end which is on the left.

Remember that part Casino royale when Bond sips his martini, realizes he’s been poisoned, then runs to his Aston Martin to inject himself with the antidote Q carefully stashed away beforehand? This is exactly the case. Except, instead of Daniel Craig (*sigh*), it’s 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, commonly referred to as the Bristol strain because it was isolated from mushroom compost in 1951 in Bristol, England.

Having a common reference species like this is undoubtedly useful for laboratories all over the world. But as with all species C. elegans accommodates genetic variability. Studies of wild strains may provide insights that would be missed if we assumed that N2 represents all worm genetics.

pha-1 is an essential gene in the N2 reference strain. N2 worms that have mutant pha-1 have pharyngeal defects (hence the name), so the gene was thought to be necessary 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; in the event that sup-35 is inactivated, it doesn’t matter if pha-1 is also deactivated. And, sup-35 overexpression mimics a loss of pha-1. The two genes clearly work against each other.

When researchers looked at the genomes of wild worms from Hawaii, they found they don’t have that pha-1. So it is clear that the gene cannot be essential for the development of worms. When they crossed males of this wild species with hermaphrodites that were N2 (that’s just how these worms work), half of the offspring died as embryos. This did not 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 fact that the N2 mother administers a toxin to 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 of the wild strain, which is why half of the progeny die in some crosses. Much other genetic evidence, both from this work and previous studies in other labs, supported this idea.

It appears that pha-1The essential function of N2 in the genetic background of N2 is not the formation of the pharynx. rather, pha-1 is needed to act as an antidote to the toxin made by N2 mothers and encoded by the sup-35 gene. That is why N2 worms with non-functional pha-1 develop OK as sup-35 is not nearby. Because 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 who don’t inherit them.” Not only is this insanely cool, but it could also have practical implications: Since these elements spread very well through populations, we might be able to hijack them to turn pathogenic vectors, such as mosquitoes, into the wild.

Of course we want to take our time with that, since we don’t really know how they work yet. However, we do know one thing: with worms, it is not only the mother who can fatally poison the brood. Ben-David’s lab previously identified another selfish genetic element, and this one had a sperm-released toxin.

Science2017. DOI: 10.1126/science.aan0621 (About DOIs).

By akfire1

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