A laboratory study at the University of California, Santa Cruz in the United States finds that the cell-cycle regulator E2F1 can restart division without broadly changing access to packaged DNA. The protein activates genes through regions that are already partly accessible. The peer-reviewed findings describe a cellular mechanism that researchers are investigating in relation to cancer.
Resting cells actively maintain their nondividing state while retaining the ability to respond to growth signals. A team working at the US-based University of California at Santa Cruz, examined how the gene-regulating protein E2F1 reactivates the cell cycle. Their laboratory study, published in The EMBO Journal, finds that it can switch on relevant genes without widespread changes in chromatin, the DNA–protein packaging inside the nucleus.[1]
Ordinary growth stimulation is accompanied by broader changes in access to chromatin. The alternative route uses regulatory regions with restricted existing accessibility. The investigators also examined interactions with nucleosomes, the protein units around which DNA is wound. These findings describe how a regulator can engage packaged genetic material as resting cells resume their cycle, rather than requiring a general opening of that packaging.[1]
Live imaging followed individual cells as E2F1 activity prompted renewed division. Without additional growth signals, cells divided at most three times, and reentry followed a protein-level threshold. The researchers are investigating whether cancer cells exploit this route. The observations concern laboratory cells and molecular interactions; identifying any therapeutic target would require establishing which cancers use the mechanism and finding suitable ways to interfere with it.[1]
