California researchers find how E2F1 triggers cell division without signals — News-Medical
Researchers at the University of California, Santa Cruz, in the United States, have found that the E2F1 protein can trigger cell division without additional growth signals. As News-Medical reports, the findings were published in The EMBO Journal.
To reproduce the exit of cells from a resting state in the laboratory, researchers usually add nutrients and growth signals. This process involves physically unpacking DNA, which is tightly packed together with proteins in the nucleus. The team confirmed that activating E2F1 can prompt cells to divide even without such additional signals.
Gene activation without DNA unpacking
The study authors found that E2F1 uses a different mechanism. The protein binds to a limited region of the genome and activates genes associated with the cell cycle. According to Associate Professor of Biomolecular Engineering Ali Shariati, E2F1 can activate these genes without significant DNA unpacking, or without it at all.
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The scientists point to the similarity of this E2F1 property to pioneer factors, which can open access to tightly packed DNA and substantially alter a cell's state. The researchers also found that cells respond to a certain threshold of E2F1 levels: after it is exceeded, resting cells begin to divide.
Possible link to cancer
E2F1 plays an important role in cell division and is disrupted in many types of cancer. At the same time, the described mechanism has limitations: without additional growth signals, cells could divide no more than three times. To observe them over time, the team used live single-cell imaging methods and DeepSea software developed in Shariati's laboratory.
The researchers suggest that cancer cells may use E2F1 activity to bypass mechanisms that keep cells in an inactive state. Next, the team plans to determine exactly how E2F1 activates genes after binding to the genome and to investigate the role of the other eight genes in this family in cancer development.
