A selfish toddler might throw a tantrum to get their way, but in worms, a “selfish” piece of DNA known as a toxin-antidote (TA) element uses something more sinister—poison. Researchers have just discovered a parent-of-origin effect with this nematode element that could be an evolutionary precursor of genomic imprinting.
Led by Alejandro Burga (Institute of Molecular Biology of the Austrian Academy of Sciences) and Eyal Ben-David (who was at the Hebrew University of Jerusalem), the altruistic team was studying two different wild isolates of C. tropicalis when they realized that they had a selfish element on their hands.
This egotistical TA consists of a toxin called slow-1 and an antidote called grow-1. When a hermaphrodite mother worm has the element in its genome, toxic slow-1 RNA is loaded into its eggs. Only those eggs that also have the TA DNA can counteract the poison with the grow-1 antidote—all other eggs develop much more slowly at a high fitness cost. That way, the selfish element ensures that it is carried on via the most fit progeny.
In a surprising twist, progeny developed normally when wild-type mothers mated with TA-carrying male worms. To the team, this looked a lot like mammalian genomic imprinting, in which some genes are repressed with methylation, depending on which parent they are inherited from. But C. tropicalis doesn’t have de novo methylases. So, upon further investigation, they found that:
- Paternal inheritance of the TA results in reduced slow-1 mRNA levels, and these effects can persist for generations—unlike imprinting, which is erased after each generation
- RNA, not protein, is responsible for the effect
- Repression of slow-1/grow-1 depends on piRNAs, which are small RNAs (sRNAs) that are part of the worm’s host defense mechanism and are important for distinguishing “self” from “non-self”
- When the mother has the TA, the toxic slow-1 mRNA gets loaded into all of the eggs and acts as a licensing agent, indicating that the TA is “self,” counteracting the piRNA defense
Because this process has some similarities with, but is not identical to, genomic imprinting, it could represent an intermediate step, which the researchers call “proto-imprinting.” TAs and similar lethal factors occur in insects, plants, and mice, so they say that interfering with sRNAs like the piRNAs could be common during the evolution of genomic imprinting.
So, choose to be selfless rather than selfish and check out the details at Nature, March 2024.
