The DNA inside our cells is constantly being damaged, and one of the worst kinds of damage is a double-strand break—when both sides of the DNA helix are cut at once. Healthy cells can normally fix these breaks using highly precise repair systems, but when those systems fail, cells sometimes resort to a less accurate backup method. Now, scientists at Scripps Research have discovered when and how this backup repair pathway gets activated, and how the process could be turned against cancer cells that rely on it to survive.

A machine learning-based resource developed at St. Jude Children’s Research Hospital predicts which intrinsically disordered regions can drive the formation of biomolecular condensates and links those proteins to RNA biology.

The nuclear pore complex (NPC) controls what moves in and out of the cell nucleus. Scientists have long debated how its flexible components team up with transport factors to create a barrier that is both fast and highly selective. Using high-speed atomic force microscopy and synthetic nanopores, the researchers showed that transport factors continuously reorganize the NPCs central transporter to enhance its selectivity and speed. The findings overturn previous rigid or gel-like models of the nuclear pore complex, offering new insight into diseases—such as cancer and neurodegeneration—that are linked to NPC breakdown. They also provide a blueprint for designing smart, nanopore-based technologies for drug delivery and filtration.