iiinova — where your digital self keeps evolving

This was true detective work—full credit to Julian @jamesjulianross.bsky.social , who persisted until he uncovered this beautiful solution to a riddle that consumed our souls for years! Huge thanks as well to our many collaborators!

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Lastly, how did KLMT-1 evolve? Turns out that a neutrally evolving beta-hairpin loop, was repurposed from a solvent exposed region of FARS-3 - in true tinkerer fashion, evolution used what was available to make a new binding interface

But how does this interaction cause toxicity? The predicted binding surface overlaps with known AIR-1 regulatory interfaces, suggesting mitosis may be dysregulated. In line with this hypothesis, we found that KLMT-1 overexpression causes various mitosis-related defects.

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To understand the reason behind this highly unusual localization, we performed an in-silico screen for interacting centrosomal proteins. And we found one - the major mitotic kinase AIR-1/Aurora A. Prediction-guided mutagenesis confirmed that this interaction is central to toxicity.

🔎 Having ruled out the most obvious explanation for toxicity , we simply asked: where does KLMT-1 localize to? Fluorescence microscopy provided a very surprising answer: KLMT-1 is enriched at the centrosome, the major mitotic microtubule organising centre in eukaryotes.

KLMT-1 is a selfish toxin that eliminates non-carrier progeny and evolved from a tRNA synthetase subunit. However, we show that KLMT-1 does not kill by interfering with the activity of the ancestral synthetase, or any global tRNA metric

Gene duplication is known to drive innovation, but how it creates profound novelty aside from minor functional adjustments is hard to envision, and even harder to find cases of. Here we identify and describe such event in a selfish toxin-antidote element from the nematode C. tropicalis. 🪱

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Manuel Irimia @mirimiam.bsky.social · 20/04/2026

🧬 New research from the Burga lab! We took a closer look at a rogue selfish protein and caught evolution in the act of turning something old into something radically new 💡 (a.k.a. neofunctionalization) @imbavienna.bsky.social www.biorxiv.org/content/10.6... Curious? Here’s a breakdown:

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Reposted by Alejandro Burga

Thrilled to present our comparative study on the evolution of zygotic genome activation (ZGA)!! 🥚🧬 Amazing PhD work of @campobes.bsky.social together with @fedemantica.bsky.social and many collaborators! @melisupf.bsky.social @crg.eu. Thread below 1/15 www.biorxiv.org/content/10.6...

biorxiv.org

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Alejandro Burga @arburga.bsky.social · 10/12/2025

muchas felicidades para ti y todo tu equipo, Alex!

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Reposted by Alejandro Burga

Mia Levine @levine-lab.bsky.social · 28/11/2025

How to keep in step when your (protein) partner speeds up… Here we investigated the adaptive remodeling of a protein-protein interaction surface essential for telomere protection. Congrats to whole team! www.science.org/doi/10.1126/...

science.org

Rapid compensatory evolution within a multiprotein complex preserves telomere integrity

Intragenomic conflict with selfish genetic elements spurs adaptive changes in subunits of essential multiprotein complexes. Whether and how these adaptive changes disrupt interactions within such comp...

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Reposted by Alejandro Burga

Jonathan Pettitt @genotripe.bsky.social · 28/11/2025

C. elegans researchers were early adopters of open science: "The development of common resources and the belief that research findings and mutant strains should be freely shared has propelled worm research to the forefront" www.pnas.org/doi/10.1073/...

pnas.org

From nematode to Nobel: How community-shared resources fueled the rise of Caenorhabditis elegans as a research organism | PNAS

Experimental organisms such as the nematode Caenorhabditis elegans are fundamental to biological discovery. The success of C. elegans research has ...

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Reposted by Alejandro Burga

Carlos Ribeiro @ribeirocarlitos.bsky.social · 26/11/2025

Thrilled to share our new paper! With @tomtom-auer.bsky.social team, we asked how #evolution reshapes what animals #eat to match their ecological niches. Using pan-neuronal Ca2+ imaging, we show that the changes are in how the brain processes #taste. Link @nature.com: www.nature.com/articles/s41...

nature.com

Evolution of taste processing shifts dietary preference - Nature

Calcium imaging of taste neurons and the ventral brain provides insight into evolutionary divergence of food choice in Drosophila species, supporting a role of sensorimotor processing in addition to p...

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Reposted by Alejandro Burga

Polina Tikanova @polinatikanova.bsky.social · 24/11/2025

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?

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Reposted by Alejandro Burga

Vienna BioCenter Scientific Training @vbcscitraining.bsky.social · 24/11/2025

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 training.vbc.ac.at/summer-school

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Reposted by Alejandro Burga

Institute of Molecular Biotechnology @imbavienna.bsky.social · 24/11/2025

🚨 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: imba.science/3M3fRyq

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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!

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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

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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.

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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!)

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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.

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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.

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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.

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