Chances are you never heard of it, but there is something else than “we” in our DNA. It sure contains our genetic information but, beyond the instructions to guide the development and function of our body, one can find small pieces of DNA with their own agenda: remains of old viruses, that have lost their capacity to leave the cell, and the so-called transposons, ancient genetic partners - or parasites - of virtually all living creatures on earth.

These genetic elements can move places in our genomes, not too often though. Some just cut-and-paste themselves onto a different position in our chromosomes, while others make many new copies and expand their numbers. In any case, every time they move there is a chance to mess with something important “for us”. Indeed, transposon mobilisation is an already known cause for some human diseases.

Considering that transposons and other related genetic elements make up almost 50% of our DNA, one should not be surprised to find that we have evolved defence systems against them. One of these systems are the PIWI-interacting RNAs (piRNA), small RNA sequences that bind to active transposons and silence them. However, many aspects of this system are still unknown.

To offer new insights into piRNA biology, a team spearheaded by Dr. Tanya Vavouri and Adrià Mitjavila, from the Josep Carreras Leukaemia Research Institute, have been studying it in mice. The research, recently published in The EMBO Journal, found that different individuals of the same species do not carry the same piRNAs.

In other words, different individuals have a different toolbox to keep parasitic genetic elements silent. What's more, the group found that the differences in the piRNA toolbox are encoded in DNA. Surprisingly, sometimes, the variation in the piRNA toolbox is itself determined by the same parasitic genetic elements that the piRNA system targets.

Fundamental research is key to having a broad understanding of the inner workings of cells. The broader the understanding, the better researchers can explain disease and, eventually, find new tools to fight back.

This research has been partly funded by the Spanish and Catalan governments, the Josep Carreras Foundation and a personal grant by La Caixa Foundation. No generative AI tools have been used in the writing of this news piece.

Research article: Eduard Casas, Adrià Mitjavila-Ventura, Pío Sierra, Cristina Moreta-Moraleda, Judith Cebria, Ilaria Panzeri, J Andrew Pospisilik, Josep C Jimenez-Chillaron, Sonia V Forcales & Tanya Vavouri. “Genetic polymorphisms lead to major, locus-specific, variation in piRNA production in mouse”. The EMBO Journal, https://doi.org/10.1038/s44318-025-00475-4