Five of 16 nominated DIGS-ILS PhD candidates received the DIGS-ILS Fellow Award 2026:
- Adelina Botezatu (Trian Chavakis Group)
- Yukta Khurana (Stefan Diez Group)*
- Karolin Küster (Mareike Albert Group)*
- Joana Marujo do Nascimento Vidigueira (Jan Brugués Group)
- Pauline Porschitz (Darja Andreev Group)
The award honours outstanding PhD candidates after the 1st year of thesis work and includes a price money of €2,000 (* split prize this year). It aims to help their research work, development of research skills, and to strengthen their research network. The allowance can be used to cover project consumables, attendance to workshops and conferences, research visits to collaborators’ labs, as well as to cover cost for a side project.
An outstanding performance during the 1st year of PhD work, along with a nomination and justification by their Thesis Advisory Committee (TAC) in the 1st AR TAC meeting is required to be eligible for the award. The predocs presented the current state of their thesis work to the DIGS-ILS Steering Committee in writing. Applications positively evaluated were invited to defend their application in a chalk talk before the committee. Detailed information on that work can be found below.
Adelina Botezatu
Elucidating molecular mechanisms of inflammation-driven arthritis
Inflammatory arthritis is a major cause of chronic pain and disability, affecting more than 500 million people worldwide. A key challenge in treating the disease is understanding how inflammation becomes persistent and leads to progressive joint damage. My PhD project investigates whether inflammation in the joint can influence immune cell productions in the bone marrow through a process known as inflammatory memory. I focus on hematopoietic progenitor cells, which give rise to immune cells and osteoclasts that contribute to inflammation and bone resorption in arthritis. Using single-cell transcriptomics and functional assays in a mouse model of inflammatory arthritis, I study how immune cell populations and their precursors change across different tissues during disease progression. By uncovering mechanisms that sustain inflammatory responses, this work aims to improve our understanding of arthritis and support the development of more effective therapeutic strategies.
Yukta Khurana
Investigating the role of microtubule lattice and tubulin post-translational modifications on bidirectional vesicular transport
Major cellular processes require trafficking of proteins, mRNA complexes, vesicles and organelles by molecular motors. Microtubule-based motors translocate a large variety of cargos often in a back-and-forth fashion which is characterized by fast runs in either direction interspersed with directional reversals. The purpose and rules governing these reversals and mechanisms by which the overall directionality is maintained remains to be elucidated. Among the key regulators of cargo transport are microtubules (MTs) themselves. Tubulin isoform diversity, MT lattice conformation, and tubulin post-translational modifications (PTMs) contribute to a “tubulin code” which could provide spatial and temporal cues for motor processivity and directionality. The project aims to unravel the role of MT lattice and PTMs like detyrosination, in bidirectional transport. Using in-vitroreconstitution assays and specifically modified tubulin, I will study vesicle motility driven by competing motor teams on MTs with defined lattice structures and PTMs. This work could provide insights into how the tubulin code regulates bidirectional cargo transport, with implications for understanding the pathogenesis of neurodegenerative disorders.
Karolin Küster
Disease modelling of Weaver Syndrome in human cortical organoids
The neocortex is central to higher cognitive functions in humans. The development of the neocortex is strictly regulated transcriptionally and epigenetically. Polycomb repressive complex 2 is an important epigenetic modifier, and mutations of its catalytic core have been linked to the developmental disorder Weaver Syndrome. Up to now, little is known about the effect of Weaver syndrome-associated protein variants on the development of the human neocortex. In this project, we aim to study early brain development in Weaver Syndrome using human cortical organoids as a disease model. Human Weaver Syndrome organoids provide, for the first time, a platform for investigating the cellular and molecular mechanisms underlying pathological changes. We are particularly interested in deciphering how abnormal epigenetic regulation affects the behaviour of neural stem and progenitor cells during human neurodevelopment.
Joana Marujo do Nascimento Vidigueira
Uncovering the role of chromatin material properties in zygotic genome activation
In the very early developmental stages of sexually reproducing species, the embryo relies on maternally-provided factors. Only after Zygotic Genome Activation (ZGA) occurs, can cells begin to differentiate into the different tissues required to generate a full organism. Despite many models having been proposed for what triggers ZGA, the regulatory mechanisms at play remain unclear. This project offers a new perspective on this problem by complementing our biochemical understanding of this process with a novel biophysical description of the genome’s material properties. To achieve this goal, we are combining optical tweezers with imaging approaches and chemical and physical perturbations of chromatin. This integrated approach could reveal a previously uncharacterised regulatory layer of ZGA.
Pauline Porschitz
The Osteoprotective Role Of Eosinophils During Homeostasis And Inflammatory Bone Loss
Eosinophils are abundant in bone marrow and secrete cytokines with anti-osteoclastogenic and pro-osteoblastogenic properties, yet their role in bone homeostasis remains poorly defined. This project demonstrates that eosinophils shape the bone marrow immune environment to suppress osteoclastogenesis and promote osteoblast lineage commitment over adipogenesis, a function evidenced by elevated osteoclast precursor gene expression and a 2.1-fold increase in bone marrow adiponectin in eosinophil-deficient ΔdblGATA mice, indicating that eosinophil loss skews mesenchymal progenitor differentiation toward adipocytes at the expense of osteoblasts. In vitro, eosinophils counteracted pro-inflammatory cytokine-induced suppression of the osteoblastogenic transcription factor Runx2 and mineralization, restoring both to baseline levels. Under inflammatory conditions in a serum-induced arthritis model, bone marrow eosinophils underwent transcriptional and metabolic reprogramming, marked by enrichment of immune-activating subsets, upregulation of alarmins S100a8/S100a9, elevated secretion of IL-33 and Pentraxin-3, and altered TCA cycle metabolism. Collectively suggesting an adaptive osteoprotective phenotype that sustains bone homeostasis during inflammatory bone loss.