Chromatin and Neurodevelopment: An Interview with Prof M. Felicia Basilicata

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We are pleased to welcome Prof M. Felicia Basilicata, who joined the Biomedical Center (BMC) of LMU Munich on the 1st of Semptember 2025 as LMU Professor of Molecular Gene Regulation. In this interview, she talks about the fascination about her research field, why some gene alterations are more common in one sex than the other - and why her lab will be attractive to future team members.

Q: Prof Basilicata, welcome to the BMC. Could you give us a short overview of your research focus?

As a postdoctoral researcher, one of my projects was to explore how the Male Specific Lethal (MSL) complex recognises its targets in the fruit fly and mouse nucleus. What began as a fundamental question soon took an unexpected turn: I discovered the first human syndrome caused by MSL mutations – Basilicata-Akhtar Syndrome. This finding revealed that these proteins act quite differently in humans compared with flies, and opened a broader set of questions about brain development and disease.

Why do mutations in seemingly unrelated genes produce such similar neurodevelopmental disorders? And why are males more frequently affected than females? These puzzles became the driving force of my research.

Today, my group investigates how genetic changes disrupt brain development, with a focus on rare neurodevelopmental syndromes. We study how alterations in chromatin regulation disturb cellular organelles across different cell types, and we search for convergent pathways that explain shared clinical features. At the same time, we explore the roots of sex-biased disease prevalence, seeking to uncover the mechanisms that make males more vulnerable to certain disorders. Our aim is to connect these discoveries into a bigger picture – revealing the common biology that underlies many neurodevelopmental conditions.

Q: What fascinates you about your research?

What really drives me: the mutations we study are incredibly rare. We are talking about 1 in 100,000 kids or even fewer. For large pharmaceutical companies, developing individual therapies just isn't feasible. But imagine if we could find a common targetable principle, a window where already-approved drugs could be repurposed to help these children. . That possibility shapes my thinking and fuels my work, because it carries real potential to bridge the gap from bench to bedside.

Q: What inspired you to move to the BMC?

I grew up scientifically in the TriRhena hub in Germany, right at the intersection of developmental and chromatin biology. As a junior fellow attending the chromatin meetings of SFB 1064, I often felt in an environment of remarkable scientific excellence. The quality of research here, the energy of the discussions, the vibrancy of this scientific community: it was infectious. When this position opened up, I knew I wanted to join this outstanding place.

Q: What methods will your team employ to explore these mechanisms?

We are method agnostic and absolutely love learning whatever technique will get us to the answer. Our toolkit includes embryonic stem cells (both mouse and human induced pluripotent stem cells), CRISPR gene editing, confocal imaging, and cutting-edge genomics. Personally, I have a particular passion for microscopy. I am highly trained in advanced imaging methods and genuinely enjoy watching phenomena in action as well as the artistry involved in visualizing and showing the minuscule world in technicolor. I very much enjoy mastering new methods or tweaking established ones to fit the needs. For our upcoming projects, we will also use lots of biochemistry and proteomics, working closely with the state-of-the-art facilities here at BMC. It's all about using the right tool for the next exciting question.

Q: What are the biggest challenges in your research field?

One major challenge is that the nucleus is traditionally seen through the lens of its core function in gene expression, but it is embedded by its very nature in the cellular space and dynamically interconnected with other organelles. This focus has limited our knowledge on how chromatin misregulation can disrupt the flow of information between compartments and how adaptive convergent pathways could lead to certain phenotypes. Also over the decades we have acknowledged sex bias in disease but often neglected to search fully for the biological mechanisms, systematically excluding sex chromosomes from large population studies while historically using only male mouse models. In my lab, I fuse these two fields, but it requires interdisciplinary approaches and coming out of comfort zones.

Q: You are currently expanding your research group. What can new team members look forward to when joining your group at the BMC?

I want to create an inclusive environment where every idea is valued, where people feel supported and energised by their work, and inspired by the thrill of discovery. Building a group that supports one another while pursuing independent projects is central to me. I like being present in the lab and especially enjoy the daily one-to-one exchanges with my team. Experiencing the realities of wet-lab experiments myself allows me to offer practical guidance when challenges arise. We embrace setbacks, both technical and conceptual, as essential parts of science – learning from them and moving towards the next opportunity.

We also aim to integrate closely with the Biophysics BMC core facility. With fresh ideas for restructuring some of their services, we hope to foster stronger collaboration and position ourselves as an active part of the infrastructure – contributing not only through our own discoveries, but by supporting and enhancing the science of others.

Interested?

The Basilicata Lab will soon advertise several job offers (PhD, Technician, Assistant and Master thesis). To learn more, please visit our career page.