International Birnstiel Award 2025: Six outstanding doctoral researchers announced

Marleen Bérouti, Ludwig-Maximilians-Universität
Supervisor: Veit Hornung

The innate immune system serves as the first line of defence against pathogens. Its ability to distinguish self from non-self is crucial for preventing harmful immune responses. Many pathogens expose their nucleic acid genome or transcriptomes during their infection cycle, which can be recognized by specialized pattern recognition receptors. Localized in the endolysosomal compartment - the entry site of many pathogens - Toll-like receptors (TLRs) 7 and 8 play a prominent role in this process. Marleen Bérouti uncovered that specific endolysosomal nucleases act cooperatively to generate TLR7-agonistic ligands. She and her collaborators also found that pseudouridine, the most common RNA modification in humans, is not efficiently processed by these nucleases into recognisable fragments and also neglected as a ligand by TLR7 and TLR8. The present findings provide an answer to the question of why pseudouridine-modified mRNA vaccines can be administered safely without triggering immune responses, a key factor in their widespread use.

Marleen Bérouti studied biochemistry at Ludwig-Maximilians-Universität in Munich (Germany), where she also pursued her PhD under the supervision of Veit Hornung. Her doctoral work was supported by the International Max Planck Research School for Molecular and Cellular Life Sciences. Bérouti is an inventor on a U.S. patent for photo-switchable PROTACs.

Featured Publication

Bérouti M., Wagner M., Greulich W., Piseddu I., Gärtig J., Hansbauer L., Müller-Hermes C., Heiss M., Pichler A., Tölke A.J., Witte G., Hopfner K.-P., Anz D., Sattler M., Carell T., Hornung V.: “Pseudouridine RNA avoids immune detection through impaired endolysosomal processing and TLR engagement.” Cell (2025). DOI: 10.1016/j.cell.2025.05.032.

Vojislav Gligorovski, EPFL
Supervisor: Sahand Jamal Rahi

Dynamic proteins that switch between functional states are vital for cellular processes, research, and therapy, but are difficult to design or evolve using existing methods. Vojislav Gligorovski devised a method for continuous in vivo evolution to optimize the properties of switchable proteins. The system was implemented in budding yeast by rewiring the cell cycle, making oscillations of a cyclin essential for cell survival. This design enabled selection for both “on” and “off” states of target proteins once per cell cycle. Moreover, selection pressure in this system was encoded by light, allowing precise temporal control. Applications of the system to optimize three important molecular tools: blue-light-responsive transcription factor, red-responsive protein-protein dimerization pair, and the doxycycline-inducible Tet-on system, uncovered new and unexpected evolutionary solutions. This research opens up new avenues for designing switchable proteins for research and therapeutic purposes.

Vojislav Gligorovski studied molecular biology at the University of Belgrade (Serbia), before moving to Switzerland for his doctoral research at the École Polytechnique Fédérale de Lausanne with Sahand Jamal Rahi. He was the top graduate of his class in Belgrade and received Serbia’s Saint Sava Award for achievements in higher education.

Featured Publication

Gligorovski V., Labagnara M., Scutteri L., Blackholm M., Möglich A., Mansouri N., Rahi S.J.: “Light-directed evolution of dynamic, multi-state, and computational protein functionalities.” BioRxiv DOI: 10.1101/2024.02.28.582517.

Jimmy Ly, Massachusetts Institute of Technology (MIT)
Supervisor: Iain Cheeseman

Humans are made up of trillions of cells and display remarkable biological complexity—far beyond that of single-celled organisms like yeast or bacteria. Yet, we have only about 20,000 protein-coding genes, just a few times more than bacteria. The answer for the origin of the complexity of living organism lies in how they use their genes: rather than producing a single protein from each gene, organisms rely on ways to produce alternative, ‘hidden’ protein variants—previously overlooked products not last of our own genome. Jimmy Ly used cutting-edge techniques to explore this hidden world. He found that these variants are precisely controlled, contribute to the diverse functions of human cells, and can even shape how genetic diseases develop. His research reveals a previously unrecognized layer of gene regulation that deepens our understanding of human biology, disease, and how complexity can emerge from a limited number of genes.

Jimmy Ly studied molecular genetics and microbiology at the University of Toronto (Canada) before joining the Massachusetts Institute of Technology in Boston (United States) for his doctoral research with Iain Cheeseman at the Whitehead Institute. Among other honours., he has been awarded the Scaringe Graduate Student Research Award of the RNA Society and the Whitehead Institute Spirit Award for Innovation.

Featured Publication

Ly J., Xiang K., Su K.-C., Sissoko G.B., Bartel D.P., Cheeseman I.M.: “Nuclear release of eIF1 restricts start-codon selection during mitosis.” Nature (2024). DOI: 10.1038/s41586-024-08088-3.

Sarah Moser, Netherlands Cancer Institute (NKI)
Supervisor: Jos Jonkers

Mutations in the BRCA1 gene greatly increase the risk of breast and ovarian cancer by disabling homologous recombination (HR), a key DNA repair process that prevents the accumulation of mutations. Sarah Moser identified a previously uncharacterized protein, FIRRM, as an important player in HR. Cells lacking FIRRM are highly sensitive to chemotherapy and PARP inhibitors (PARPi), drugs commonly used to treat HR-deficient cancer, suggesting that testing for FIRRM mutations may help predict treatment success. She also discovered a new mechanism of therapy resistance. PARPi do not just damage DNA but also disturb DNA packaging by removing histones, the proteins that cover and organize our DNA. Blocking the recycling of these histones creates additional stress and kills tumour cells, even if they were previously resistant. Together, this work deepens our understanding of DNA repair and proposes new strategies to improve the treatment for HR-deficient cancers.

Sarah Moser studied food science and biotechnology at the University of Natural Resources and Life Sciences in Vienna (Austria), followed by molecular medicine at Erasmus University in Rotterdam (Netherlands). She then joined the Netherlands Cancer Institute in Amsterdam for her doctoral research with Jos Jonkers, supported by a prestigious Boehringer Ingelheim PhD Fellowship.

Featured Publication

Moser S.C., Khalizieva A., Roehsner J., Pottendorfer E., Kaptein M.L., Ricci G., Bhardwaj V., Bleijerveld O.B., Hoekman L., van der Heijden I., di Sanzo S., Fish A., Chikunova A., Haarhuis J.H.I., Oldenkamp R., Robbez-Masson L., Sprengers J., Vis D.J., Wessels L.F.A., … Jonkers J.: “NASP modulates histone turnover to drive PARP inhibitor resistance.” Nature (2025). DOI: 10.1038/s41586-025-09414-z

Shirsha Saha, Indian Institute of Technology, Kanpur
Supervisor: Arun Kumar Schukla

G-protein-coupled receptors (GPCRs) represent the largest class of cell surface receptors in the human genome. These receptors perceive a wide array of chemically divergent stimuli and play crucial roles in a broad range of physiological processes in our body. They constitute the largest family of drug targets for many human disorders with nearly one third of the currently prescribed medicines modulating their activities in cellular context. Activation of GPCRs by their natural agonists typically leads to their signalling through two distinct signal-transducers, the heterotrimeric G-proteins and β-arrestins. However, some GPCRs may exert preferential engagement with one of these two signal-transducers leading to pathway-selective downstream responses referred to as biased signalling. Shirsha Saha’s research added to our understanding of the molecular basis of ligand recognition, receptor activation, and transducer-coupling for selected 7TMRs in the context of biased signalling and functional divergence using cellular, pharmacological, and structural approaches.

Shirsha Saha studied biotechnology at St. Xavier’s College in Kolkata (India) before joining the Indian Institute of Technology Kanpur for her doctoral research with Arun Kumar Shukla. During her PhD she was awarded a Prime Minister’s Research Fellowship. Saha is now a postdoctoral associate at the University of Rochester Medical Center in the United States.

Featured Publication

Saha S., Khanppnavar B., Maharana J., Kim H., Carino C.M.C., Daly C., Houston S., Sharma S., Zaidi N., Dalal A., Mishra S., Ganguly M., Tiwari D., Kumari P., Jhingan G.D., … Shukla A.K.: “Molecular mechanism of distinct chemokine engagement and functional divergence of the human Duffy antigen receptor.” Cell (2024). DOI: 10.1016/j.cell.2024.07.005.

Eric Sun, Stanford University
Supervisor: Anne Brunet

As we age, the cells in our brains change in ways that can lead to neurodegenerative diseases and cognitive decline. To better understand these changes, Eric Sun created a spatial map that profiled gene expression for individual cells in the mouse brain across lifespan. Using machine learning, he built “spatial aging clocks” that can track a cell’s biological age based on its gene expression. These clocks revealed that some cells accelerate aging in their neighbours—like T cells, which promote aging—while others, like neural stem cells, seem to slow it down. Eric Sun also developed new tools to uncover the specific pathways driving these effects. For example, T cells may promote aging through inflammation, while stem cells may release helpful factors that protect brain health. This research provides a detailed single-cell portrait of the aging brain and raises the possibility that targeting specific cells could slow brain aging.

Eric Sun studied chemistry and physics at Harvard University (United States), where he graduated summa cum laude and received the Sophia Freund Prize for the highest academic achievement in his class. He then pursued graduate studies in applied mathematics at Harvard before joining Stanford University for his doctoral research with Anne Brunet and James Zou.

Featured Publication

Sun E.D., Zhou O.Y., Hauptschein M., Rappoport N., Xu L., Navarro Negredo P., Liu L., Rando T.A., Zou J., Brunet A.: “Spatial transcriptomic clocks reveal cell proximity effects in brain ageing.” Nature (2025). DOI: 10.1038/s41586-024-08334-8.

Honourable Mentions

As in previous years, the selection committee faced a high number of outstanding nominations, and many strong candidates could not be acknowledged with an award. The selection committee highlighted an additional six scientists from the shortlist as “honourable mentions” to give them special recognition:

Lukas Teoman Henneberg, Max Planck Institute of Biochemistry
Research field: Ubiquitin signaling
Supervisor: Brenda Schulman and Matthias Mann

Rebeka Butković, University of Bristol
Research field: Membrane trafficking
Supervisor: Peter Cullen

Shiyi Lin, Westlake University
Research field: Structural biology of ion channels
Supervisor: Zhen Yan

Erez Yirmiya, Weizmann Institute of Science
Research field: Microbiology and virology
Supervisor: Rotem Sore

Nell Saunders, Université Paris Cité and Institut Pasteur
Research field: Virology
Supervisor: Olivier Schwartz

Ervin Ascić, Lund University
Research field: Cancer immunotherapy
Supervisor: Carlos-Filipe Pereira
 

About Max Birnstiel and the Birnstiel Foundation

Max Luciano Birnstiel (1933 – 2014) was a molecular biologist and founding director of the Research Institute of Molecular Pathology (IMP). In this role, he made a major contribution to the exceptional academic standing of the IMP. He retired from his post as director in 1996.

Birnstiel’s research focused on gene regulation in eukaryotes. His lab was the first to purify single genes, the ribosomal RNA genes from the frog Xenopus laevis, in the late 1960s. Birnstiel was one of the first scientists to study how gene expression is regulated. He is also recognised for one of the earliest discoveries of a gene enhancer element, which his lab published in 1980. As a science manager, Birnstiel was a visionary who not only set the IMP on track to achieving research excellence, but he was also a vital force behind raising the profile of the Vienna BioCenter, now one of Europe’s most dynamic life science hubs with more than 2,800 people from 80 countries, working in over 135 research groups and more than 35 biotech companies.

Throughout his life, Max Birnstiel was a supporter of young talent and fostered an egalitarian culture at the IMP. It was in this spirit that a foundation bearing his name was set up in 2018. The Max Birnstiel Foundation co-funds initiatives and activities that support young scientists in molecular life sciences, such as the Vienna BioCenter Summer School and the International Birnstiel Award for Doctoral Studies in Molecular Life Sciences. ww.maxbirnstiel.org, www.imp.ac.at/birnstiel-award

See these and all past awards...