IMP: Six emerging scientists receive the International Birnstiel Award 2026
The 2026 International Birnstiel Award for Doctoral Studies in Molecular Life Sciences has named its laureates — the eighth cohort since the award was established in 2019. This year's selection drew 109 nominations from institutions around the world. Six researchers have been chosen: Joe Dobbs (European Molecular Biology Laboratory), Maximilian Madern (Hubrecht Institute), Hannah Tam (Harvard University), Stephen Tang (Columbia University Medical Center), Abigail Xie (Sloan Kettering Institute), and Zhejing Zhang (Kyoto University).
The selection panel’s assessment of this year’s pool of nominees left no doubt: “We were again overwhelmed by the quality of the nominees,” said one member. “Reading through all these nominations of brilliant people makes you want to go straight to your lab and get up to gear.” The response reflects a broader truth about the award: in eight years, the calibre of candidates has never ceased to impress as the Birnstiel Award’s reputation continues to grow.
The 2026 cohort adds two novelties to the award’s history. Zhejing Zhang becomes the first laureate affiliated with a Japanese institution — a strong sign for the award’s global reach. And Maximilian Madern’s selection means that the research group of Marvin Tanenbaum at the Hubrecht Institute has become the first lab that has produced two Birnstiel Award winners (after Sanne Boersma in 2021), something no other research group has achieved to date.
The laureates will be celebrated at a ceremony in Vienna on 4 November, where each will receive a certificate, a trophy, and a prize of 2,000 Euros. The Birnstiel Award accepts one nomination per institution or PhD programme annually; calls go out each May through the IMP website, social media, and a dedicated campaign. The award is a joint initiative of the Max Birnstiel Foundation and the Research Institute of Molecular Pathology (IMP), the institute where Max Birnstiel served as founding director.
Joe Dobbs, European Molecular Biology Laboratory (EMBL)
Supervisor: Julia Mahamid
The process of gene expression, where DNA is transcribed into mRNA by RNA polymerase and then translated into proteins by the ribosome, is central to every living organism. The regulatory mechanisms involved are diverse and depend on the specific cellular and environmental context. Joe Dobbs investigated how these interconnected systems operate by examining individual bacterial cells with a transmission electron microscope. He combined this technique with advances in image analysis, AI, and structure prediction to identify molecules and analyse their structures at high resolution. His work demonstrated how entire molecular cycles can be studied within their functional cellular contexts. Using this approach, he made several fundamental discoveries about how the molecular machinery of gene expression is coordinated. These findings shed light on bacterial translation initiation, the coupling of transcription and translation, ribosome attachment to membranes, and viral infection.
Joe Dobbs studied microbiology at the University of Victoria (Canada), graduating with honours in 2020. He then joined the European Molecular Biology Laboratory (EMBL) in Heidelberg (Germany) for his doctoral research with Julia Mahamid, graduating summa cum laude. Prior to his PhD, he worked at the MRC Laboratory of Molecular Biology (LMB) in Cambridge (United Kingdom). During his doctorate he completed a competitive internship at Genentech. Dobbs is now a postdoctoral fellow with Erin Schuman at the Max Planck Institute for Brain Research in Frankfurt.
Maximilian Madern, Hubrecht Institute
Supervisor: Marvin Tanenbaum
Ribosomes are complex molecular machines in our cells that build proteins. They read mRNA, a temporary copy of genetic information from DNA, and use it as a template to synthesize proteins. Although several ribosomes often translate the same mRNA at the same time, it was unclear whether they influence one another during translation. Maximilian Madern developed a new microscopy technique that allows individual ribosomes to be observed at work inside living cells. Using this method, he found that ribosomes frequently come into close contact and collide with one another. Rather than always being harmful, these collisions can be beneficial: when a ribosome stalls on a difficult mRNA sequence, a following ribosome can help it rapidly become “unstuck” and continue translating. Madern calls this phenomenon “ribosome cooperativity”, a process in which ribosomes support one another to promote fast and efficient protein synthesis.
Maximilian Madern studied molecular biotechnology at FH Campus Vienna (Austria) and molecular biology at the University of Vienna, receiving his master's degree with distinction in 2018. He then joined the Hubrecht Institute in Utrecht (Netherlands) for his doctoral research with Marvin Tanenbaum. His work received the CS&D (Cancer, Stem cell and Developmental biology) PhD Programme Best Publication Award in 2025.
Hannah Tam, Harvard University
Supervisor: Ya-Chieh Hsu
Regeneration is challenging for mammals. When skin is injured, it scars. Although the wound closes, many skin cell types, including hair follicles, sweat glands, blood vessels, pigment cells, and fat, are lost. Consequently, skin can no longer regulate temperature or relay sensory information. By contrast, skin injured before birth can regenerate these diverse cell types, thereby rebuilding functional skin without scarring. Why regeneration disappears after birth, and whether it can be restored, were unknown. Hannah Tam discovered that regeneration is not lost but blocked. By comparing wounds before and after birth, she identified a fibroblast population in mice unique to wounds after birth that produces CXCL12, a signal that attracts excessive nerves to the wound. By removing CXCL12 or reducing neuronal activity, she found that skin injured after birth can regenerate diverse cell types, restoring functional and scarless skin. This work identifies a major barrier to scarless regeneration and provides opportunities for regenerative therapies.
Stephen Tang, Columbia University Medical Center
Supervisor: Samuel H. Sternberg
Bacteria are under constant attack by viruses called bacteriophages, and over billions of years have evolved many strategies to survive infection. Stephen Tang examined an unusual family of bacterial defence systems that use reverse transcriptase enzymes to generate antiviral DNA molecules during infection. While DNA usually serves as a stable record of genetic information, the transient DNA molecules produced by these systems have alternative roles. In one system, they harbour transient “hidden” genes that, once expressed, produce toxic proteins that halt viral replication. In another, the DNA products themselves trigger cell death to limit further viral spread. Tang’s work also uncovered an unexpected evolutionary link between these bacterial enzymes and telomerase, the central enzyme responsible for maintaining chromosome ends in humans and other eukaryotes.
Abigail Xie, Sloan Kettering Institute
Supervisor: Lydia Finley
Metabolism allows cells to convert nutrients into energy and molecules required to sustain life. At the heart of metabolism is the tricarboxylic acid (TCA) cycle, a pathway that provides cellular energy and metabolic intermediates. Abigail Xie identified a previously unappreciated function of the TCA cycle: metabolite clearance. She and her collaborators discovered that when cells produce citrate at high levels, catabolising citrate in the first step of the TCA cycle becomes essential to maintaining cell fitness in an array of cancer cells and organs. This work shows that, beyond the traditional outputs of the TCA cycle, nutrient clearance is an additional essential function of the TCA cycle required to sustain cellular health in specific contexts.
Zhejing Zhang, Kyoto University
Supervisor: Mineko Kengaku
During brain development, neurons migrate from the sites where they are produced to those where they function. Their nuclei are squeezed as they move through dense brain tissue. Zhejing Zhang found that this squeezing induces transient DNA double-strand breaks (DSBs). Unlike in many cancer cells, where DSB formation is triggered by nuclear envelope (NE) rupture, NE rupture was rare in migrating neurons. Instead, confined migration leads to the accumulation of stalled topoisomerase IIβ on the genome. The stalled enzyme is subsequently removed through proteasomal degradation, and the resulting DSBs are repaired through the non-homologous end joining (NHEJ) pathway. Disrupting this pathway resulted in prolonged DNA damage, altered gene expression in the cerebellum, and motor deficits in mice. These findings suggest that migration-induced DSBs are part of neuronal development and that their successful repair plays an important role in brain development and function.