Happy to share that my PhD project is finally published!🪱✨
Selfish genes are found across the tree of life. They can disrupt inheritance patterns and at the same time act as units for molecular innovation. Here we tried to answer one big question: how do selfish genes emerge in the first place?

The Vienna BioCenter Summer School 2026 call is now open for talented undergrads, it's a great opportunity for students who are interested in graduate study in the life sciences. Georg Busslinger from CeMM is recruiting! Please share
https://training.vbc.ac.at/summer-school/

🚨 New paper alert!

Scientists in the Burga lab show for the first time how toxin-antidote elements—selfish genetic elements that perpetuate by poisoning those embryos that don’t inherit them—evolved from normal cellular proteins. More: https://imba.science/3M3fRyq

Polina drove this project and made the critical observations that revealed the entire evolutionary path. I couldn’t be prouder (also, she’s my first student!). Polina is on the job market, and any lab would be incredibly lucky to have someone with her talent!

So grateful to all our collaborators (Ben-David & Dong Labs) and lab members who helped drive this project. But I especially want to thank Polina Tikanova @polinatikanova.bsky.social @imbavienna.bsky.social @oeaw.bsky.social @vbcscitraining.bsky.social

Our results also uncover an even deeper principle. Nematode and plant F-box proteins are thought to engage in arms races with parasitic elements. In this conflict, accidental targeting of self-proteins is inevitable—making the birth of selfish genes a by-product of innate immunity.

This interaction suppressed the toxicity of future paralogs via ubiquitin-mediated degradation, allowing alleles to persist long enough to evolve selfish behavior. These results also support the idea that novelty can arise largely through neutral steps (positive selection is not always the answer!)

What triggered this recurrent shift in function? All the evidence points to a fortuitous binding event: a fast-evolving F-box protein latched onto the tRNA synthetase.

To tackle this, we studied selfish genes segregating in wild populations of the nematode C. tropicalis. There, we found that a core gene—a tRNA synthetase essential from bacteria to humans—gave rise to three independent toxin–antidote selfish systems in a single species.

This question is surprisingly hard to answer. Selfish genes evolve rapidly in an arms race with host defenses, obscuring their origins. And their earliest steps often involve deleterious alleles that should be purged by selection—making the rise of selfishness both unlikely and paradoxical.

www.nature.com/articles/s41...

🪱 Selfish genes are everywhere and drive some of biology’s biggest innovations (CRISPR, antibody recombination, epigenetics). Yet almost no one asks the obvious question: how does a selfish gene begin? Our new manuscript uncovers how selfishness can emerge directly from the host genome.

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