Every cell in the body must carefully protect its DNA to stay healthy. To do this, cells coordinate several essential tasks, such as turning genes on and off, processing genetic information, and repairing damaged DNA. These activities occur within the cell nucleus, in small, flexible structures known as biomolecular condensates, which function as temporary workspaces without physical walls.
This research project will explore how flexible parts of proteins—regions that lack a fixed shape—help create and control these workspaces. These flexible protein regions influence how condensates form, how they behave, and how well they perform important functions in gene control and DNA repair.
The study will focus on two important systems. The first involves a protein called EWS and its cancer‑related variant, EWS::FLI1, which disrupts normal gene regulation and contributes to cancer development. The second system centers on the BRCA1‑BARD1 protein complex, which helps repair damaged DNA and whose activity is regulated by gene expression and DNA damage signals.
To answer these questions, the research team will use a combination of advanced laboratory techniques that allow scientists to observe proteins at the molecular level and in living cells.
By understanding how specific features of flexible proteins control these DNA‑protecting structures, this research aims to explain how cells normally maintain genome stability—and what goes wrong in diseases such as cancer and neurodegenerative disorders when these systems fail. The findings are expected to deepen our understanding of how the cell nucleus is organized and may help guide the development of new treatments that target abnormal protein behavior in human disease.