Our work is driven by the hypothesis that cellular form is not merely a reflection of function, but one of its determinants. In the developing cortex, neural progenitors extend complex protrusions that shape how they sense their environment, receive proliferative cues, generate neurons and allow neuronal migration. We investigate how these morphological features are established, how they influence developmental potential, and how they contribute to the extraordinary expansion of the human neocortex.

We are particularly interested in basal radial glia, neural progenitors that underpin human cortical expansion and are a hallmark of primate brain development. These progenitors show striking morphological diversity and we investigate how distinct morphotypes relate to proliferative capacity, transcriptional identity and cell fate. We further aim to define the molecular machinery that governs basal radial glia morphogenesis and to determine how its disruption leads to disease. We ask how altered progenitor architecture changes neurogenesis, cortical growth and developmental trajectories. This work provides a mechanistic framework for understanding how defects in stem cell morphology contribute to neurodevelopmental disorders, such as Down syndrome, and developmental features of cancer predisposition syndromes, like neurofibromatosis-1.

To address these questions we employ spatial biology across scales. We combine high-resolution imaging, including time-lapse microscopy, with spatial transcriptomics, genome editing and computational analysis across complementary model systems, from animal models to human fetal tissue and cortical organoids. By integrating dynamic cell behaviour with molecular identity and function, we aim to reveal how progenitor morphology becomes developmental determinant. Through this research, we seek to advance our understanding of cortical development through the lens of cell morphology and to uncover principles that link human brain complexity to its vulnerability in disease.

Our work is driven by the idea that, as in development, cellular form is not merely descriptive, but functionally instructive. We have shown that in glioblastoma, the most aggressive brain tumor, stem cells display striking morphological heterogeneity and that this diversity reflects functionally distinct tumor behaviors rather than transient variation. Our goal is to define the morphoregulatory machinery that enables glioma stem cells to adopt clinically relevant cellular states. We investigate how distinct stem cell morphologies shape proliferation, self-renewal, invasion into healthy brain tissue, resistance to chemotherapy and interaction with their microenvironment.

We ask how specific morphologies support not only communication between tumor cells, but also interactions with neurons, blood vessels and immune cells, thereby shaping invasion, survival and therapeutic response. We also extend this framework to gliomas arising in the cancer predisposition syndrome neurofibromatosis type 1, asking how altered cellular states and morphoregulatory mechanisms contribute to tumor initiation and progression in genetically vulnerable contexts. This work positions cell morphology as a new layer of tumor heterogeneity and a potential entry point for therapeutic intervention across aggressive and predisposition-associated gliomas.

To address these questions, we integrate spatial biology with functional assays. Across patient-derived tumor organoids and assembloids, tumor samples and in vivo models, we pair high-resolution live imaging, spatial transcriptomics, calcium imaging, electrophysiology, functional genetics and computational analysis to link cellular architecture with transcriptional identity and disease-relevant behaviors. By integrating perturbation screens, dependency-map approaches and validation in physiologically relevant systems, we aim to uncover morphoregulatory vulnerabilities that can be used to predict, limit and ultimately disrupt tumor progression and recurrence. Through this research, we seek to advance our understanding of glioma biology and open new avenues for precision therapies in glioblastoma and neurofibromatosis type 1-associated gliomas.