Researchers from the University of Basel have uncovered the mechanism of cell rupture during programmed cell death, challenging the traditional view of cells simply bursting. Their study, published in Nature, reveals that the protein ninjurin-1 triggers this rupture by assembling into filaments that act like a zipper to compromise the cell membrane. This process is crucial as it allows for the elimination of damaged or infected cells, helping to prevent tumor growth and the spread of pathogens.
The team utilized advanced techniques, including sensitive microscopy and NMR spectroscopy, to observe ninjurin-1’s role at an atomic level. Instead of collapsing like a balloon due to osmotic pressure, ninjurin-1 creates specific breaking points in the membrane. Initially, two ninjurin-1 proteins cluster and drive a wedge into the membrane, leading to the formation of larger lesions as additional proteins attach, ultimately resulting in cell disintegration.
These findings enhance understanding of cell death and may inform future therapies, particularly for cancer and neurodegenerative diseases, where manipulating cell death processes could be beneficial. The study signifies a critical advancement in the field of cellular biology.
