The layer of cells lining internal organs is like a crowd in a packed subway: everyone stands shoulder to shoulder, but sometimes the crowd starts to flow, and people slip past each other. Biologists call this behavior a transition from a jammed, solid state to a fluid one. Until now, it was thought that the key was cell shape: if cells become more elongated, the tissue liquefies. That's like people in a queue sticking out their elbows and squeezing through.

New work shows that this is not necessarily true. The researchers took a layer of cells and weakened the proteins that glue them together — a kind of molecular adhesive at the junctions. The tissue became noticeably more fluid, and cells slid past their neighbors more easily. But their shape did not change: no change in elongation, size, or packing density. Nor did the tension at contact points change. So cells liquefied while remaining geometrically the same.

To explain this, the scientists proposed treating the cell glue not only as a force that pulls edges together but also as a source of friction. When cells slide, adhesion molecules catch on each other and create viscous resistance, like honey between your palms. Incorporating this friction into a mathematical model allowed them to accurately reproduce the experimental results. Now it is clear that tissue fluidity depends on the balance between how strongly cells are glued and how much that glue impedes their movement.

This is important not only for fundamental science. Our body's tissues constantly remodel: during wound healing, cells crawl over the damaged area; during embryonic development, layers change shape. And in cancer, tumor cells detach from their neighbors and start to migrate, and perhaps it is precisely the weakening of adhesion without a change in shape that triggers this dangerous process. Understanding how cells become fluid could suggest ways to intervene in these scenarios.