Cell division is necessary for multicellular organisms, but uncontrolled division leads to cancer. Problems such as DNA damage during division can cause mutations. Cells have checkpoints that ensure everything goes well, but even after passing them problems can arise.
Mitosis that lasts too long, during which copied chromosomes separate, may indicate damage. Previous studies have shown that retinal cells can sense slow mitosis and stop dividing. A new study by scientists in Japan and San Diego shows that this behavior extends beyond retinal cells. They called this system the “mitotic stopwatch.”
Cells depend on proteins. An important protein, p53, stops division when problems occur. During slow mitosis, p53 forms a complex with two other proteins (mitotic chronometer). Mutations that prevent the formation of this complex stop the chronometer. The complex forms only during prolonged mitosis and remains stable by being transferred to daughter cells. Scientists discovered a specific kinase (PLK1) that is required for the formation of the complex. They believe that PLK1 slowly replaces the protein during mitosis, allowing the complex to form. If mitosis occurs quickly, the complex does not have time to reach a high level and has no effect. However, during slow mitosis the complex accumulates and persists in daughter cells, stabilizing p53 and potentially stopping future divisions.
Interestingly, all three proteins together are tumor suppressors, and mutations in them increase the risk of developing cancer. The researchers confirmed that the mitotic chronometer was often inaccurate in tumor samples. This discovery reveals how cells retain memories of past problems with division.
Source: Ferra
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