Excited to be in Paris for #Yeast2025! I’ll be presenting Poster #35 this afternoon, stop by to check out our latest work on how nutrient levels shape compensatory evolution under replication stress. Would love to chat!

I don't like the person I become when designing primers

Enjoyed this @natrevcancer.nature.com article on comparative oncology - how we can learn from other species 🐘🐋🦜🐍 about ways to prevent (& possibly treat) cancer. Both a review and a call to action for the research community. www.nature.com/articles/s41... @atjcagan.bsky.social @cmaley.bsky.social

@mariananatalin6.bsky.social @marcofumasoni.bsky.social show evolutionary repair in response to DNA replication stress in yeast is predictable and consistent across different environments #CompensatoryEvolution #NutrientAvailability #ReplicationStress #GxE ➡️ www.embopress.org/doi/full/10....

Happy to be the next (and 1st female) @crg.eu director. The CRG always stood out to me, for its excellence in understanding life's principles, with implications for health and biodiversity, & its collaborative, open and innovative way of doing science. Thrilled to join its amazing community in 2026!

Huge thanks to the reviewers, @reviewcommons.org and @molsystbiol.org for their rigorous and very constructive feedback! (7/7)

These findings support the idea that compensatory evolution—at least under chronic replication stress—is not only reproducible, but remarkably robust to environmental variation! (6/7)

We also uncovered a new player in adaptation to replication stress: Med14, a component of the RNA Pol II mediator complex. A single amino acid change repeatedly emerged and improved fitness, putatively by tuning transcription and chromosome cohesion. (5/7)

Here’s the plot twist: We observed that while nutrient availability influenced the rate of adaptation, it didn't alter the nature of adaptive mutations. Mutations in just four genes explained most of the fitness recovery and were consistently selected across all environments. (4/7)

We evolved 48 yeast populations experiencing chronic replication stress across different glucose levels. It turns out glucose starvation alleviates the physiological defects of these mutants. (3/7)

How does the environment, particularly nutrient levels, shape evolution when essential processes like DNA replication are impaired? A classic #GxE question—with implications for cancer biology and drug resistance. (2/7)

Excited to share the first paper of my PhD with @marcofumasoni.bsky.social ‬, now published in @molsystbiol.org 🥳! We explored how nutrient levels influence adaptation to perturbed DNA replication. Here’s what we learned 🧵👇 www.embopress.org/doi/full/10....

We also uncovered a new player in adaptation to replication stress: Med14, a component of the RNA Pol II Mediator Complex. A single amino acid change repeatedly emerged and improved fitness, putatively by tuning transcription and chromosome cohesion. (5/7)

Here’s the plot twist: We observed that while nutrient availability influenced the rate of adaptation, it didn't alter the nature of adaptive mutations. Mutations in just four genes explained most of the fitness recovery and were consistently selected across all environments. (4/7)

We evolved 48 yeast populations experiencing chronic replication stress across different glucose levels. It turns out glucose starvation alleviates the physiological defects of these mutants. (3/7)

How does environment, particularly nutrient levels, shape evolution when essential processes like DNA replication are impaired? A classic #GxE question—with implications for cancer biology and drug resistance. (2/7)

🎺Please RT! We have a funded #Postdocposition in our lab at @IGCiencia in Portugal 🇵🇹🇪🇺! Come and join us in exploring the wonders and evolution of genome maintenance processes, and engage with the extended #LifeScience community in #Lisbon! Details here: fumalab.github.io/join