54 compounds affecting pancreas development: Using an image-based screen and a robust analysis pipeline, researchers screened hundreds of molecules and identified 54 compounds that change pancreas organoids shape and/or cell types.

Generating functional human pancreatic acinar cells: Researchers focused on the compounds that inhibit the GSK3A/B protein and drive pancreatic progenitor cells to differentiate into pancreatic acinar cells. A further optimization of the growth media enabled the progenitor cells to develop into fully functional acinar cells.

Possibilities for pancreatic cancer research: The ability to generate acinar organoids is valuable for future studies on pancreatic exocrine function and cancer initiation in humans, as acinar cells are thought to be an important cell of origin for pancreatic cancer.

Organoids are three-dimensional miniature models of organs, grown in a dish. They have become a valuable tool for studying human development, organ regeneration, function, and disease progression. Organoids derived from patient tissues or created through cell and genetic engineering allow researchers to investigate how specific proteins or their variants affect these processes.

However, current approaches to studying multiple genes at once have limitations. They don’t provide a complete picture of how cells change shape and move around in response to genetic and molecular changes. High-content image-based screens provide a better solution for this, but their implementation and analysis pose difficulties.

Researchers in the group of Anne Grapin-Botton, director at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, Germany, and also honorary professor at TU Dresden, along with the MPI-CBG Technology Development Studio, have now developed a system to test many different compounds (molecules) at the same time using pancreatic organoids, consisting of human pancreatic progenitor cells. With high-content image-based screening – a way of taking detailed pictures of the cells in the organoids – and quantitative multivariate analysis to analyze the data from these pictures, the researchers were able to identify changes in the cells.

From sphere to rosette shape

“Through the screening of 538 compounds, we found 54 compounds that had a significant effect on the pancreas progenitor organoids. I especially focused on compounds that affected cell identity as well as the shape of organoids and identified inhibitors of the GSK3A/B protein. When this protein is inhibited, the WNT signaling pathway is activated, leading to the expression of genes found in acinar cells. Though we saw an increase of those genes with the inhibition of GSK3A/B, the cells did not fully differentiate into acinar cells. To achieve our goal to differentiate acinar cells, we optimized the medium in which the cells grow,” explains Rashmiparvathi Keshara, the lead author of the study and former doctoral student in the group of Anne Grapin-Botton.

“We observed that removal of the growth factor FGF led to further differentiation of our organoids and formation of rosette-like structures. We were very happy to see this, as the self-organization and formation of these structures is a characteristic of acinar cells in the living organism,” says Karolina Kuodyte, another author of the study and a postdoctoral researcher in the Grapin-Botton group.

Functional pancreatic acinar cells

With electron microscopy, the researchers found tiny vesicles inside the cells that are a typical feature of enzyme-producing pancreatic acinar cells. They then tested the functionality of acinar cells, confirming they were indeed producing functional enzymes, such as amylase and trypsin, which are important for digestion.

“Acinar cells are thought to be a main contributor to pancreatic cancer. We are really excited to present a protocol for developing human acinar cells with unprecedented functionality in a human pancreas organoid,” says Anne Grapin-Botton, who oversaw the study. “Our simple protocol with very few components to differentiate acinar cells has the potential to advance our understanding of pancreas development and may lead to the discovery of new therapeutic targets for pancreatic cancer.” The researchers plan to further assess human pancreatic cancer initiation using their system.

Tissue engineering the pancreas: Working with three-dimensional pancreatic models (organoids), derived from mouse cells, researchers combined computer simulations with experiments to find out what controls the shape of lumens (fluid-filled cavities) during the development of the pancreas.

Proliferation, Pressure, Permeability: The shape of the lumen depends on the balance between the cell proliferation rate and the pressure in the lumen. Low pressure and high proliferation produce more complex or ‘star-shaped’ lumens. The pressure in lumens remain low because the surrounding pancreatic tissue is permeable.

Implications for organ development and disease: The discovered mechanisms can be potentially relevant to other organs with complex ductal systems and to common cystic diseases. Furthermore, these findings could be used to develop new therapeutic strategies, including testing the effects of drugs for diseases.

Organs often have fluid-filled spaces called lumens, which are crucial for organ function and serve as transport and delivery networks. Lumens in the pancreas form a complex ductal system, and its channels transport digestive enzymes to the small intestine. Understanding how this system forms in embryonic development is essential, both for normal organ formation and for diagnosing and treating pancreatic disorders. Despite their importance, how lumens take certain shapes is not fully understood, as studies in other models have largely been limited to the formation of single, spherical lumens. Organoid models, which more closely mimic the physiological characteristics of real organs, can exhibit a range of lumen morphologies, such as complex networks of thin tubes.

Researchers in the group of Anne Grapin-Botton, director at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, Germany, and also Honorary Professor at TU Dresden, teamed up with colleagues from the group of Masaki Sano at the University of Tokyo (Japan), Tetsuya Hiraiwa at the Institute of Physics of Academia Sinica (Taiwan), and with Daniel Rivéline at the Institut de Génétique et de Biologie Moléculaire et Cellulaire (France) to explore the processes involved in complex lumen formation. Working with a combination of computational modeling and experimental techniques, the scientists were able to identify the crucial factors that control lumen shape

Star-shaped lumen resembles real panceas

“Three-dimensional pancreatic structures, also called pancreatic organoids, can form either large spherical lumen or narrow complex interconnected lumen structures, depending on the medium in the dish,” says Byung Ho Lee, postdoctoral researcher in the group of Anne Grapin-Botton and lead author of the study. “By adding specific chemical drugs altering cell proliferation rate and pressure in the lumen, we were able to change lumen shape. We also found that making the epithelial cells surrounding the lumen more permeable reduces pressure and can change the shape of the lumen as well.”

“Our model can measure and predict which parameters account for the transitions of the lumen shapes, enabling feedback into the experiments themselves” says Kana Fuji, doctoral student in the research group of Masaki Sano. To understand how individual cells grow and divide and how this affects the formation of the lumen, the research team used a mathematical model in addition to the experiments to simulate the process.

“Our study shows that the shape and structure of the lumen in pancreatic organoids depend on three main factors: how fast cells proliferate, the pressure inside the lumen, and how permeable the cells around the lumen are,” says Anne Grapin-Botton, who supervised the study together with Byung Ho Lee. “This discovery could help us understand how other organs with narrow interconnected ducts develop and how common cystic diseases affect them. Our model system could further research in the field of organ development and tissue engineering and also potentially be used to test how different drugs affect diseases, which could lead to new treatments. This could help us better understand and treat diseases that affect the pancreas and other organs with branching ducts.”

In most species, cells divide by forming a contractile ring of actin at the cell equator. This ring contracts like a purse-string, pinching the cell’s contents to result in two new cells. Although the ‘purse-string’ model of cell division is observed in many organisms, this is not the case for species with very large embryonic cells such as sharks, platypus, birds and reptiles. In these cases, the actin ring cannot fully close due to the cell’s immense size and large yolk sac. How exactly cell division takes place in these organisms remained an open question in the field, until now. “With such a large yolk in the embryonic cell, there is a geometric constraint. How does a contractile band, with loose ends, remain stable and generate enough force to divide these huge cells?” asked Alison Kickuth, a recently graduated PhD student from the Brugués group at the Cluster of Excellence Physics of Life (PoL) and lead author of the study. Their experiments, published in a seminal new study in Nature, have found an answer to this question.

The scientists studied zebrafish embryos, which divide rapidly and share the characteristic of having large, yolk-filled cell during early development. By precisely cutting the actin band with a laser, Alison observed that the band continued to ingress despite being severed, suggesting that anchoring points were distributed along the band, rather than at the ends. In addition, it seemed that microtubules, another essential part of the cytoskeleton, appeared to bend and splay in response to the laser cuts, and had a critical role in stabilizing the band during contraction. To clarify the role of microtubules in this process, the authors disrupted them in two separate experiments: by chemically inducing depolymerization (effectively stopping new microtubules from forming), and by physically disrupting them using an obstacle, in the form of a microscopic oil droplet. Without microtubules, the actin band collapsed, proving that microtubules are essential for holding the band in place, and provided both mechanical support and signalling during its formation.

Changes in the cytoskeleton are known to happen in other species as cell cycles progress. Importantly, the cell cycle is separated into distinct phases of activity; a mitotic phase (M-phase) where the DNA is divided, and interphase, where a typical cell grows and replicates its DNA. After DNA has been divided, large structures made of microtubules called asters grow to span the entire cytoplasm. These asters are essential during interphase for deciding where the actin band will form and start contracting, marking the future cleavage plane. Given that microtubules are known to stiffen the cytoplasm in various cellular contexts, the authors sought to explore if asters would contribute to stiffening to help anchor the actin band. To investigate, the authors employed magnetic beads and observed their displacement under magnetic forces. These experiments allowed the scientists to measure changes in cytoplasmic stiffness during cell cycle stages. They found that the cytoplasm becomes stiffer during interphase, acting as a scaffold to stabilize the actin band. In turn, it becomes more fluid during M-phase, allowing the band’s ingression between the two future cells. These dynamic changes in stiffening and fluidization play a key role in the division process.

Only one question remained: How did the band remain stable throughout M-phase despite the cytoplasm becoming more fluid-like? By imaging the ends of the actin band over time, the team observed that although the band is unstable during M-phase while contracting, it did not collapse fully. Instead, this retraction is “rescued” due to the fast cell cycles in these early stages. In the following interphase when the cytoplasm stiffens again due to the asters reappearing, the band becomes re-stabilized. Then, the actin band continued ingressing during the next fluid-phase. These cycles of instability during M-phase and stabilization during interphase repeated over several cell cycles until division was complete. This alternating pattern acts like a ‘mechanical ratchet’, driving cell division without needing a fully-formed contractile ring. In this case, division is possible through the alternating material properties of the cytoplasm, and takes place over multiple cell cycles instead of just one.

“The temporal ratchet mechanism fundamentally alters our view of how cytokinesis works”, emphasized Jan Brugués, corresponding author of the study. This finding provided an effective solution for early cell divisions in cells that were too large for conventional cell division, and have rapid cell cycles. “Zebrafish are a fascinating case, as cytoplasmic division in their embryonic cells is inherently unstable. To overcome this instability, their cells divide rapidly, allowing ingression of the band over several cell cycles by alternating between stability and fluidisation until division is complete” highlighted Alison regarding this finding. This discovery represents a novel paradigm for understanding cell division in large embryonic cells and may apply broadly across species with yolk-rich embryos. Additionally, this study highlights temporal control of material properties in the cytoplasm as an important contributor to cellular processes, a role that may be expanded in future studies. Understanding these mechanisms will open new perspectives for studying development in different species.

PoL Press release: https://physics-of-life.tu-dresden.de/news/2026/01/07/the-mechanical-ratchet-a-new-mechanism-of-cell-division-uncovered

Nearly three centuries ago, a Swiss mathematician, Leonhard Euler, laid the mathematical foundations for describing such instabilities by explaining the buckling of an elastic line at a critical value of the compressive force. Centuries of work by other mathematicians and scientists built upon Euler’s ideas to describe more complex buckling instabilities. One seemingly innocuous question remained open, though: How does a compressed line buckle within a curved surface?

Pierre Haas, research group leader at the Max Planck Institute for the Physics of Complex Systems (MPIPKS), the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), and the Center for Systems Biology Dresden (CSBD), and Shiheng Zhao, doctoral student in the group of Pierre Haas, have now answered this question that Euler did not solve: Combining exact and numerical calculations, the researchers discovered that the mathematical structure of the mechanical instability changes fundamentally within a curved surface.

“We found that buckling happens differently if the line is constrained to a curved surface: the critical force for the instability is zero, so the line starts bending even at small compressive forces. However, as we keep compressing the line, it snaps suddenly to a higher compression and bends even more,” says Shiheng Zhao.

These theoretical results are the foundations explaining a class of elastic instabilities within curved surfaces that also has biological relevance. Shiheng Zhao and Pierre Haas, together with colleagues from Princeton and the Flatiron Institute, have recently shown that the morphogenesis of the hindgut of the fruit fly Drosophila can be explained by an analogous mechanical instability within a curved surface.

While buckling instabilities are classical marks of material failure in engineering applications, this and related mechanical instabilities have only been recognized more recently as an important mechanism for the emergence of shape in developmental biology. “Our findings can help us understand how tissues composed of many cells develop into organs and organisms, because the mechanical forces that drive development often act on curved, rather than flat, tissues,” Pierre Haas therefore concludes.

Three-dimensional multicellular human liver model: For the first time, a 3D human organoid model, developed with liver tissue from patients, consists of three liver cell types, derived from adult hepatocytes, cholangiocytes, and liver mesenchymal cells.

Retaining structure and function: The novel complex organoid models, or assembloids, reconstruct essential structural and functional features of the human periportal liver region and have patient-specific traits. They capture key aspects of human liver physiology in a dish, including drug detoxification and metabolism.

Liver disease investigation: When manipulated, this human periportal liver model can mimic several characteristics of biliary fibrosis. It provides a platform to study liver diseases in humans, accelerate the development of new drugs, enable early diagnosis, and advance personalized medicine.

Liver disease is a major global health problem, causing over two million deaths worldwide each year. While animal models have helped to understand liver biology, they often fail to accurately translate to human biology. Due to the liver’s unique architecture, existing human models fail to replicate the complex interactions between different cell types in the liver and accurately show how diseases progress. Existing tissue-derived liver organoid models consist of only one cell type and fail to replicate the complex cellular composition and tissue architecture, such as the liver periportal region. Complex 3D multicellular models that capture human liver portal cellular interactions do not exist for adult human liver tissue yet. This limits the ability to study liver disease and develop new treatments.

Previous liver models

The research group of Meritxell Huch, director at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, Germany, and also Honorary Professor at TU Dresden, started to address this issue in a previous study in 2021 (Dynamic cell contacts between periportal mesenchyme and ductal epithelium act as a rheostat for liver cell proliferation, Cordero-Espinoza, Lucía et al., Cell Stem Cell, Volume 28, Issue 11, DOI), where the researchers developed a liver organoid consisting of two cell types, cholangiocyte and mesenchyme cells, but still lacked other periportal cell types – most importantly hepatocytes, the cells that build the majority of liver mass. In 2025, the research group of Meritxell Huch was able to create a next-generation organoid model, composed of three liver cell types of the mouse – adult hepatocytes, cholangiocytes, and liver mesenchymal cells – to reconstruct the mouse liver periportal region. (Mouse periportal liver assembloids recapitulate mesoscale hepatic architecture and biliary fibrosis, 29th May 2025, Nature, DOI)

Developing a multicellular human liver model

In the recent study, published in the journal Nature, researchers from the group of Meritxell Huch, together with colleagues from the group of Andrej Shevchenko at the MPI-CBG, from the group of Daniel Stange at the Carl Gustav Carus University Hospital (UKD) Dresden and the National Center for Tumor Diseases (NCT/UCC), and from the groups of Daniel Seehofer and Georg Damm at the Clinic for Visceral, Transplant, Thoracic, and Vascular Surgery at the Leipzig University Medical Center, developed a patient-specific human periportal liver assembloid. This advanced liver model features adult human cholangiocytes, liver mesenchymal cells, and hepatocytes, which were derived from 28 patients. It contains multiple cells, which are combined together in a process similar to LEGO. Once assembled, the cells self-organize into 3D structures that reproduce in vitro the cellular arrangements and cell-cell interactions of the tissue in vivo.

Developing the liver model was real teamwork. It involved not only the experimental scientists from the Huch lab and clinicians from Leipzig and Dresden but also bioinformaticians and technical assistants from the different labs. One of the four lead authors, Yohan Kim, a former postdoctoral researcher in the Huch group and now an assistant professor at Sungkyunkwan University in Suwon, South Korea, says, “When we received the tissue from the patients, we first had to separate the individual cell types and expand them in a dish before combining them again. I researched the culture conditions for the cells to grow before being assembled, prior to my departure for my new position at Sungkyunkwan University.” The tissue from the patients was provided by the Carl Gustav Carus University Hospital (UKD) in Dresden and the Clinic for Visceral, Transplant, Thoracic, and Vascular Surgery at the Leipzig University Medical Center. With the support of the research technician Robert Arnes-Benito, the culture conditions were further optimized into what are now the final culture conditions to expand human hepatocytes.

Sagarika Dawka, a doctoral student and another lead author of the study, continued the work of Yohan by finding conditions to mature the cells in vitro. She says, “I was able to develop the liver model further, so it featured bile canaliculi, which drain into the bile duct in the liver periportal region. When this bile drainage system is disrupted, it causes liver damage and disease. This is why it was so important for our liver models to include bile canaliculi. The present study is the first complex human liver model outside of the body that has bile canaliculi.”

Lei Yuan, a postdoctoral researcher and one of the lead authors, then worked on combining the cells to make the periportal assembloids. First, he labeled the different cells (liver mesenchymal cells and cholangiocytes) in order to be able to track them once combined. Then, he found the right conditions to induce their self-assembly.  “Additionally, I optimized the periportal assembloid protocol from the assembly method to the media that the cells were growing in. The proper medium is essential for promoting the cells' growth and differentiation,” says Lei.

Another lead author of the study, Anke Liebert, a postdoctoral researcher, was mainly responsible for the molecular and functional characterization of the liver models. “I was looking at how well the models were performing their function. I tested how well our liver models function compared to normal human liver cells. With the help of computational biologist Fabian Rost, I tested that the models correctly captured the gene expression of the living tissue.”

With their existing liver models, the group created a living biobank of hepatocyte organoids from 28 patients, which can be frozen and thawed to reinitiate cultures when needed.

Personalized medicine and drug development

The novel human liver model shows patient-specific traits and retains essential structural and functional features of the human periportal liver region. “We overcame a major challenge with our new model. Reconstructing the multicellular periportal liver tissue organization and cellular interactions outside of the living body hasn’t been possible so far. With our models, we can build and control different parts of the liver in a lab. This helps us understand how different cells and their surroundings work together to create a healthy liver, and, when these interactions are wrong, how diseases like biliary fibrosis arise,” says Meritxell Huch, who oversaw and supervised the study. “Our new liver models have the potential to change the way we study and treat liver diseases. They could help us develop new diagnostic tests, test the safety of new medicines, improve drug toxicity assessment, and create personalized treatments for patients with liver diseases.”

“For over 40 years, thousands of mice are bred with genetic mutations. But often, despite breeding many mice, none of the offspring have the desired mutation,” explains Ronald Naumann. “In line with the 3R principles to reduce the number of animals for research, replace them with alternative methods, and refine their treatment, we have developed a new way to test sperm from mice predictably for desired genetic mutations. This method is based on a special analysis test, the STR (Short Tandem Repeat) procedure, which enables fast and reliable identification of genetic characteristics. As a result, only offspring that are of scientific interest for the respective experiment are bred. The approach allows mice to be bred efficiently without the need for large numbers of additional animals. This has already allowed us to reduce the number of mice that were bred by around 5,600 over the past four years.”

© Ronald Naumann

Ronald has been working with laboratory animals since 1995 and established the Transgenic Core Facility at the MPI-CBG in 2002. Furthermore, he played a key role in establishing many facilities worldwide and continues to support international scientific institutions with his broad expertise.

The basis for this new technology was the following publication: Novel insights into the genetic background of genetically modified mice. Dobrowolski, Fischer, Naumann, Transgenic Res. 2018. DOI

 News article of the 3Rs Collaborative:  https://3rc.org/award-winners/

“I really felt the energy of the MPI-CBG right away and knew when I entered the building that there's just a different vibe here,” says Madalena Reimão Pinto. “I am looking forward to working with many different colleagues at the MPI-CBG and on the Dresden campus. For example, the close link to the Center for Systems Biology Dresden (CSBD) and their expert mathematicians enables me to start thinking of questions that I just didn't even dare to think of before.”

Madalena Reimão Pinto studied Cell and Molecular Biology at the New University of Lisbon and then undertook her MSc studies in Human Molecular Genetics at Imperial College London. Afterwards, she worked as a technician at the University of Lisbon for 1.5 years and for 6 months at the MRC-LMB in Cambridge, UK. For her PhD, Madalena moved to Vienna to the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA). In 2019, she started her postdoc at the Biozentrum of the University of Basel. In 2019, she received an EMBO Postdoctoral Fellowship, in 2021 a Marie Skłodowska-Curie Postdoctoral Fellowship, and in 2024, a research fund for excellent junior researchers from the University of Basel. As of November 2025, Madalena is a research group leader at MPI-CBG.

“It's amazing that neural stem cell research has a long history in Dresden and that we have very well-organized facilities here at MPI-CBG that enable us to model those mutations in complex tissues,” says Matthias Muhar. “I'm also very keen on learning organoid biology here at the institute. Cerebellar organoids and cerebral organoids will be my main organoid system.”

Matthias Muhar studied biology at the University of Vienna and finished his PhD in 2018 in molecular biology at the Institute of Molecular Pathology (IMP), also in Vienna. During his PhD, he worked on the development of genetic and transcriptomic tools for the study of gene regulation in leukemia. In 2018, he received the Life Science Research Award of the Austrian Association of Molecular Life Sciences and Biotechnology. Matthias moved to Zürich in 2019 to work as a postdoctoral researcher at ETH, where he looked at the end of gene expression and what happens when gene products, proteins, are removed by cells. As of November 2025, Matthias is a research group leader at MPI-CBG.

With this award, the Signal Transduction Society recognizes Theresia’s scientific excellence in the field of signal transduction, demonstrated by her contributions to understanding insulin action during her PhD and immune sensing of nucleic acids in her postdoctoral work.

She received the prize at the 28th STS Meeting in Weimar, where she presented her latest research and delivered the laudatory speech for this year’s STS Honorary Medal Awardee Hao Wu (Harvard Medical School & Boston Children’s Hospital), who was a Valle Visiting Professor at MPI-CBG in 2025.

Theresia studied biology at the Humboldt-Universität of Berlin. After research stays at ETH Zurich and the University of Helsinki, she completed her PhD in the laboratory of Ünal Coskun at TU Dresden, where she discovered the mechanism underlying insulin receptor activation. She joined Anthony Hyman’s group at MPI-CBG in 2020 and shifted her research focus to nucleic acid-induced immune signalling and higher-order assemblies. In her postdoctoral work, she established a new research topic in the lab funded by the Walter Benjamin Programme of the German Research Foundation (DFG) and the NOMIS Foundation. She also discovered a mechanism by which the SARS-CoV-2 virus antagonizes innate immune recognition.

Congratulations!

“EMBO is delighted to welcome the new young investigators. Their outstanding achievements demonstrate the excellence and ambition that will drive progress in the life sciences. We are pleased to support these young group leaders as they take the next steps in their careers, and we look forward to their discoveries and contributions to our community,” says EMBO Director Fiona Watt.

As part of the Young Investigator Programme, Jesse Veenvliet has access to a wide range of benefits, including training and mentoring opportunities, as well as access to core facilities at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany. Young investigators also receive a financial award of 15,000 euros, can apply for additional grants, and gain support for networking activities, such as joint group meetings or travelling to conferences.

Jesse Veenvliet and his group reconstruct development in a dish to understand how embryos build themselves. By guiding pluripotent stem cells to self-organize into stem-cell-based embryo models (embryonic organoids), the team investigates how cells sense and use their physiological microenvironment to sculpt the body plan with remarkable robustness. “I’m thrilled to join this lively and inspiring network. The EMBO YIP community brings together an incredible group of talented and passionate researchers across disciplines, and I’m excited about the opportunities this opens for me, my team, and our work,” says Jesse Veenvliet.

EMBO is an organization of more than 2,100 leading researchers that promotes excellence in the life sciences in Europe and beyond. The major goals of the organization are to support talented researchers at all stages of their careers, stimulate the exchange of scientific information, and help build a research environment where scientists can achieve their best work. The administrative EMBO headquarters is in Heidelberg, Germany.

EMBO press release: https://www.embo.org/press-releases/twenty-eight-group-leaders-become-embo-young-investigators/

EMBL Council selected Anthony A. Hyman as next Director General: In his new role, Hyman will be responsible for overall leadership, strategic direction, and management of the European Molecular Biology Laboratory (EMBL).

Mandate will commence on 31 March 2026: Hyman will assume his role at the EMBL in Heidelberg in April 2026, taking over EMBL’s leadership from Interim Director General Peer Bork and Interim Executive Director Ewan Birney.

At its winter meeting, the Council of EMBL selected Anthony A. Hyman, who is currently a Director at the Max Planck Instititute of Molecular Cell Biology and Genetics (MPI-CBG), as EMBL’s next Director General. Hyman’s mandate will begin on 31 March 2026, when he will take over EMBL’s leadership from Interim Director General Peer Bork and Interim Executive Director Ewan Birney.

“I am pleased to announce the decision by the EMBL Council to elect Anthony Hyman as future EMBL Director General,” says Peter Becker, EMBL Council Chair. “Tony witnessed the spirit of EMBL early on in his splendid career. He is a visionary and experienced scientist, who is very well suited to leading EMBL as it continues to innovate and build on its strong foundations.”

“I will be joining EMBL as its next Director General at a moment when the life sciences are changing rapidly, and when the institute’s role across Europe has never been more important,”  says Hyman. “New technologies are giving us access to molecular, cellular, and tissue-level information at a precision and scale that simply did not exist a decade ago. Together with modern computational approaches, including AI, this creates a real opportunity to connect molecular mechanisms to the organisation of cells and tissues in ways that were not possible before.

Hyman continues, "My new position will greatly benefit from the expertise I gained at MPI-CBG, where I was one of the founding directors in 1998.  Everyone needs some luck in life, and mine was to be given the opportunity to move to Dresden and be involved in founding this institute. It has been an honor to be part of building this institute in Dresden, and I would like to express my gratitude to all my colleagues at MPI-CBG and to the Max Planck Society for these fulfilling 25 years."

“This is a great opportunity for Tony, and we are happy to see him take on this new challenge," says Stephan Grill, Managing Director of the MPI-CBG. “At the same time, Tony will be deeply missed here at MPI-CBG. He has been a key part of our success as one of the founding directors. But, we are looking forward to the chance to strengthen the connections between MPI-CBG and EMBL in the future!”

Hyman is one of four founding directors of, and group leader at, the MPI-CBG in Dresden, Germany. He held the role of the institute’s Managing Director from 2010-2013 and from 2021-2023 and currently also holds a Professorship of Molecular Biology at Technische Universität Dresden, Germany. 

From 1993 to 1999, Hyman was a Group Leader and Visiting Senior Scientist at EMBL Heidelberg. He studied Zoology at University College London before moving to the Laboratory of Molecular Biology, MRC in Cambridge, England for his doctoral research. He obtained his PhD in 1988 (awarded by King’s College, Cambridge University), and completed a postdoctoral fellowship at the University of California San Francisco, USA. 

Hyman’s research focuses on unravelling the intricacies of biological condensates and phase separation in health and disease. Biomolecular condensates are a class of membrane-less organelles that carry out different functions within the cell. The research group of Anthony Hyman studies how phase separation impacts the formation of such membraneless compartmentalisation of macromolecules inside living cells. Understanding how and why condensates form and how they can transform into irreversible protein aggregates has important relevance for studying neurodegenerative diseases like ALS and Alzheimer’s disease. 

His research has received some of the highest accolades, including the EMBO Gold Medal (2003), the Gottfried Wilhelm Leibniz Prize (2011) for his work on microtubules and cell division, the Körber European Science Prize (2022), and the Breakthrough Prize in Life Sciences (2023) for discovering a fundamental mechanism of cellular organisation mediated by phase separation of proteins and RNA into membraneless liquid droplets. Hyman is a Fellow of the Royal Society (2007) and is an elected member of EMBO (2000), the Academia Europaea (2014), the National Academy of Sciences (2020), the German National Academy of Sciences Leopoldina (2021), and the Austrian Academy of Sciences (2023). 

Press Release of EMBL: https://www.embl.org/news/people-perspectives/embl-council-announces-next-embl-director-general/

Mertixell Huch, who is also a Honorary Professor at TU Dresden, focusesses on fundamental principles underlying the maintenance and repair of adult tissues, as well as the mechanisms by which their dysregulation contributes to disease. Her research includes 3D organoid models of the stomach, liver, and pancreas, aiming to unravel critical insights into tissue regeneration and pathology. Anthony Hyman, who has also been recognized as a Clarivate Citation Laureate earlier this year, discovered a fundamental mechanism of cellular organization mediated by phase separation of proteins and RNA into membraneless liquid droplets.

Analysts from the Institute for Scientific Information (ISI) at Clarivate recognized 6,868 individuals with 7,131 awards from more than 1,300 institutions in 60 countries and regions. The evaluation and selection process draws on data from the Web of Science Core Collection and uses quantitative metrics and qualitative analysis to identify individuals whose work has had a genuine, global influence on their fields.

Clarivite Press Release: https://clarivate.com/news/clarivate-announces-highly-cited-researchers-2025-list/

The field of biomolecular condensates has seen a sharp increase in the number of related research publications. To help organize this vast information, the CD-CODE database and encyclopedia was created in 2023 by the research group of Agnes Toth-Petroczy at the Max-Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) and at the Center for Systems Biology Dresden (CSBD). The CrowDsourcing COndensate Database and Encyclopedia (CD-CODE.org) is a platform collecting knowledge on the biomolecular condensates based on experimental data, enhanced by a crowd-sourcing functionality to engage condensate experts.

Since first being published in 2023, CD-CODE has been very valuable in advancing research and has even been used to develop new tools predicting proteins that form condensates. Additionally, condensate protein components are now cross-referenced in the UniProt Protein Database and information in CD-CODE is linked to other databases to enhance its utility in research.

CD-CODE is an example of interdisciplinary collaborative teamwork between computational and experimental biologists and software engineers. With input from researchers of several groups at the MPI-CBG and the CSBD, such as from the group of Anthony Hyman and the Scientific Computing Facility at MPI-CBG, the researchers in the Toth-Petroczy group developed CD-CODE 2.0 together with Diana Mitrea from Dewpoint Therapeutics. This enhanced version expands the utility of CD-CODE 1.0 for biomedical research. The two lead authors, Ksenia Kuznetsova and Maxim Scheremetjew, explain, “New features such as data on nucleic acid condensate components, infectious condensates, condensate-regulating drugs, and disease-linked condensate abnormalities expand CD-CODE’s utility for biomedical research and hypothesis generation. We also addressed the usability of CD-CODE 2.0 with improved search capabilities, convenient programmatic access, and relationship-based architecture to enable interconnectivity across major biomedical databases.”

Agnes Toth-Petroczy concludes, “CD-CODE 2.0 will make it easier to use computational tools and data analysis to study biomolecular condensates. The upgrade will make CD-CODE a more useful tool for many different fields of science, such as biomedical research, and will help connect research on condensates to new treatments and therapies.”

Scientists at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), the Helmholtz-Zentrum Dresden-Rossendorf (HZDR), and the École Polytechnique Fédérale de Lausanne (EPFL) have developed new tools to get mechanistic insights into ether lipid biology. 

The research team used chemically modified ether lipids with two distinct reactive groups. Those so called bifunctional lipids allow to visualize ether lipid localization and study their interaction with proteins for the first time. 

A combination of fluorescence imaging, machine learning-assisted image analysis, and mathematical modelling revealed unique transport mechanisms of individual ether lipids.

“Using our new tools, we discovered that non-vesicular transport is the main mechanism for ether lipid transport,” explains Kristin Böhlig, who led the study. She continues, “However, some ether lipid types are transported faster than others, suggesting the presence of specific, so far undiscovered lipid transport proteins that can distinguish between ether lipid types.”

These results imply that the cellular lipid handling machinery is capable of identifying even small structural differences in ether lipids, adding to the evidence supporting the biological significance of lipid diversity.

“Our bifunctional ether lipid probes provide a flexible toolkit for studying ether lipid biology in detail. This will have significant benefits for understanding the functions of ether lipids in fundamental cell biology and their role in human diseases,” says André Nadler, who oversaw the study. “Studying ether lipids in mechanistic detail may in the future help to develop new treatments for diseases that are caused by imbalances in lipid metabolism.”

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“I knew that Heather Harrington, a director here at MPI-CBG, is building a community to connect math with biology. Since I deeply enjoy working with applications, I thought Dresden could be a good place to continue this work. And here I am, and I am excited to be here.” says Daniela Egas Santander.

Daniela did her bachelor's degrees in chemical engineering and mathematics at the Universidad San Francisco de Quito in Quito, Ecuador. She went to the University of Copenhagen afterwards for a master's and PhD in algebraic topology. She went to the École polytechnique fédérale de Lausanne (EPFL) in Switzerland for a postdoctoral fellowship in applied mathematics, focusing on applications to neuroscience at the laboratory of topology and neuroscience.  Afterwards, she continued working at the Blue Brain Project, which aimed to build biologically detailed brain simulations to deepen our understanding of brain function. As of October 1st, Daniela is a research group leader at the MPI-CBG and the CSBD.

Metabolism constantly maintains a flux of energy and matter that is vital to cells, so scientists speculated that thermodynamics imposes fundamental constraints on life's ability to sustain itself. Thermodynamics states that, first, energy can only change form, not be created or destroyed. Second, whenever energy is utilized, part of it must be wasted—degraded to a form that cannot be used anymore. This means that organisms must be careful: they need to expend energy to grow, but if they waste too much, they may be left without it. However, how organisms utilize energy to grow and how growth is constrained by thermodynamics remain largely unknown.

Researchers in the group of Jonathan Rodenfels at the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, Germany, and in the group of Pablo Sartori at the Gulbenkian Institute for Molecular Medicine in Oeiras, Portugal, sought to understand how the laws of thermodynamics influence cellular growth. The team realized that a black-box type of approach might be the key to solving this problem. This approach—common in bioengineering—allows researchers to work with minimal information. It cannot describe how energy is processed inside the cell, but it enables us to calculate how much energy is wasted.

Tommaso Cossetto, the lead author of the study and a former postdoctoral researcher in the Rodenfels and Sartori groups, explains, “We applied this method to a large set of data from many different published studies and used it to quantify how much energy is dissipated or wasted by microbes as they grow. We then used nonequilibrium thermodynamics—a theory from physics—to analyze this data.”

Their study, published in Nature Communications, identifies two thermodynamic rules governing the growth and energy utilization of single-celled organisms, including archaea, bacteria, and yeast. Different types of microorganisms waste about the same amount of energy to grow a unit of biomass. This is the case whether they use oxygen, inorganic molecules, or fermentation as a metabolic strategy to grow. As a second rule, however, the team found that the use of oxygen requires more energy to produce biomass. This makes aerobic respiration, the process by which a cell uses oxygen to grow, a more efficient way for cells to grow than anaerobic respiration or fermentation, as the energy wasted is a smaller proportion of the energy required.

“Our two empirical rules constitute a long-sought-after connection between metabolism and thermodynamics,” say Jonathan Rodenfels and Pablo Sartori, who oversaw the study. “We found that there are fundamental limits to how cells can grow and function. Our findings are based on observations and data, but we don't yet understand the molecular and mechanistic reasons behind these limits. Further research will help us understand how cells work and how they can be improved or optimized.”

“Dresden has a very tight connection of experiments and theory, which made it a really attractive place for me,” says Fridtjof. “The Max Planck Society is a wonderful place to focus on science, and I think it's a real privilege to have that freedom. There are many research groups here that I would love to collaborate with in the future, and I'm really looking forward to exploring new research directions here.”

Fridtjof Brauns studied physics and theoretical and mathematical physics at the Ludwig Maximilian University (LMU) in Munich. He also pursued his PhD at the LMU and went from there to the Kavli Institute for Theoretical Physics at the University of California-Santa Barbara for a postdoc with Boris Shraiman and Cristina Marchetti, where he focused on questions in development, cell- and tissue mechanics as well as active matter.

Proteins are the central molecules of life. Although the human genome codes for approx. 20,000 different proteins, there are countless variants of them. How this diversity comes about, how proteins take on their specific functions in the body – and what happens when errors occur during protein production – is investigated by Agnes Toth-Petroczy, using a novel interdisciplinary approach.

A particular focus of her research is on intrinsically disordered proteins, proteins that lack a fixed structure and therefore are difficult to analyze in conventional biochemistry. They account for up to 30 percent of the human proteome, and their function has been little understood. Moreover, she studies phenotypic mutations – errors during protein production in the cell (transcription and translation errors), which are not part of the genome. This is a broad field that has been little researched so far, but is of great importance for understanding the evolution of proteins and their role in various disease patterns.

Her current projects also analyze the collective organization of proteins into biomolecular condensates, little droplets within the cell where proteins interact with other proteins. Her research shows how such “meeting points” emerge, how they have changed in the process of evolution, and what role erroneous proteins could play in this process.

By developing innovative computer-based models and tools, she enables systems-biological investigations into previously difficult-to-access phenomena, with applications for both academic basic research to understand protein evolution and clinical applications.

“Agnes Toth-Petroczy is an exceptionally creative scientist who breaks new ground by using in-depth and innovative methodologies to reveal previously hidden dimensions of life at the molecular level,” said Max Löhning, Chairman of the Foundation Council of the Schering Stiftung, in recognition of the prize winner’s achievement.

By launching the Schering Young Investigator Award, the Schering Stiftung upgrades its tradition of promoting young talents for the 21st century. The award succeeds the Friedmund Neumann Prize and acknowledges the global nature of science. The 10,000-euro Young Investigator Award will be awarded on November 24, 2025, during a festive award ceremony at the Berlin-Brandenburg Academy of Sciences and Humanities.

About the Award Winner

Agnes Toth-Petroczy studied chemistry at Eötvös Loránd University in Budapest, Hungary, specializing in theory and computation and developing a special interest in intrinsically disordered proteins. She completed her PhD in life sciences in the lab of Prof. Dan Tawfik at the Weizmann Institute in Israel, where she studied the principles of protein evolution. As recipient of an EMBO postdoctoral research fellowship, she joined the lab of Debora Marks at Harvard Medical School (USA) where she developed computer-based methods to predict the structures of disordered proteins. She subsequently switched to translational research and worked as instructor in medicine at the Division of Genetics of the Brigham and Women’s Hospital in Boston, contributing to several novel gene-disease relationships. Since 2018, she has headed the “Protein plasticity and evolution” research group at the MPI-CBG and the CSBD. She is a member of the DFG-funded “Physics of Life” Cluster of Excellence at TU Dresden, an EMBO Young Investigator, and a recipient of an ERC Starting Grant.

Press Release of the Schering Stiftung