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Cell Memory in Mitosis: A Complex System Revealed
When discussing memories within biology, the focus typically shifts to the brain and the processes occurring in neurons. However, beyond the complexities of the brain, cells themselves also possess memory systems. Cells retain information regarding their developmental history, exposure to pathogens, and various other factors. An intriguing question arises: How do cells manage to carry information across multiple divisions?
There is no singular answer to this question, and the specifics of such memory systems are challenging to decipher. Nonetheless, recent research has shed light on a distinct memory system within cells. Specifically, cells can remember instances where their parent cell encountered challenges during division, often linked to DNA damage and the onset of cancer. Consequently, if the division process faces significant issues, the resulting daughter cells may cease to divide further.
Cell Division Regulation and the Mitotic Stopwatch
In multicellular organisms, cell division remains meticulously regulated to prevent uncontrolled proliferation characteristic of cancer. However, various challenges during the division process, such as DNA replication, damage repair, and chromosome distribution, can lead to mutations. Notably, cells incorporate numerous checkpoints throughout division to ensure the accurate completion of each step.
While passing through these checkpoints may indicate the cell’s readiness to proceed, recent findings suggest that challenges can persist post-division. Mitosis, the stage where chromosomes separate into daughter cells, could potentially introduce damages if extended. Prior evidence indicated that certain retinal-derived cells could halt division if mitosis duration exceeded normal limits.
Recent collaborative investigations conducted in Okinawa and San Diego unraveled this phenomenon, revealing that it extends beyond retinal cells to become a broader response marking slow mitosis in cells universally. Precise timing experiments showcased a direct correlation: longer mitosis durations heightened the likelihood of subsequent daughter cells ceasing division. This characteristic behavior was termed a “mitotic stopwatch” by the researchers.
Mechanisms Underlying the Mitotic Stopwatch
How does a cell internally regulate a mitotic stopwatch mechanism? The intricate network primarily involves a crucial protein, p53, known for its pivotal roles in cellular damage detection and division control. The researchers uncovered that during mitosis, p53 forms a complex with two additional proteins—ubiquitin-specific protease 28 and p53-binding protein 1. Disrupting this protein complex via mutations halted the functioning of the mitotic stopwatch.
Notably, the subsequent stabilization of this complex post-mitosis ensured its transmission to daughter cells, facilitating their ability to halt division if necessary. The researchers pinpointed the involvement of a kinase, specifically PLK1, which phosphorylates the proteins to initiate complex formation. Chemical inhibition of PLK1 highlighted its indispensable role in activating the mitotic stopwatch mechanism.
This orchestrated process culminates in the stabilization of p53 levels, subsequently impeding future cell divisions upon reaching significant thresholds. Additionally, all proteins within the complex are established tumor suppressors, emphasizing their roles in mitigating cancer risks. Consistent observations of defective mitotic stopwatches in tumor samples authenticated the proposed mechanisms.
The distinct mitotic stopwatch mechanism exemplifies how cells retain memories of challenging division experiences. However, this system represents only one facet of cell memory storage, interlinking with myriad intricate pathways that regulate cellular activities. While efficiently addressing specific issues related to division, such mechanisms are intricately woven into a complex network governing cellular functions.
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