Every second, many cells in our bodies split to make new cells. This process is essential for life and needs thousands of tiny parts working together perfectly. Sometimes, things go wrong.
Before a cell can split, it must copy all of its DNA so each new cell gets a full set of instructions. If the DNA is copied correctly but the cell does not finish the split, the result is one cell with twice the usual amount of DNA. Scientists call this whole genome duplication, or WGD.
Think of it like printing two copies of a paper and then putting both copies into the same folder instead of separating them.
Researchers have known that having extra DNA can cause many problems. The cell may stop working, become inactive, die, change into another type, gather damage over time, or help diseases such as cancer grow.
Two Ways Cells Can Miss the Split
A team at Hokkaido University wanted to see if the reason a cell fails to split changes what happens later. They looked at two common causes of whole genome duplication: failure of cytokinesis and mitotic slippage.
In cytokinesis failure, the cell goes through almost all of division but stops short of the final cut that separates the two new cells. In mitotic slippage, the cell begins division but exits the process too early, before its chromosomes are properly divided.
Both mistakes leave the cell with double DNA, but the scientists found that the outcomes are very different.
Why Some Double‑DNA Cells Keep Living
Using live‑cell movies and special labels that highlight chromosomes, the researchers followed what happened after each type of error.
Cells that resulted from cytokinesis failure were generally stable and had a higher chance of surviving. Cells that came from mitotic slippage often showed uneven chromosome distribution and died more often.
The key difference was how the chromosomes were arranged.
During mitotic slippage, chromosomes were frequently split unevenly, creating a serious genetic imbalance that lowered the cell’s chances of survival. In cytokinesis failure, chromosomes stayed more evenly divided, which helped the cell stay stable.
When the scientists experimentally improved chromosome separation in the mitotic‑slippage cells, those cells became much more viable.
What This Means for Cancer Research
Whole genome duplication is common in cancer cells, and some cancer treatments can unintentionally cause it. Cells that survive with extra DNA can keep growing and may lead to tumor return.
The new findings suggest that targeting the ways chromosomes separate could stop abnormal cells from surviving and spreading.
“Different ways of causing whole genome duplication have been ignored for a long time,” said researcher Uehara. “We compared cells made by each method and found that they behave very differently over time.”