Video: The researchers filmed the mouse embryos developing over time using a microscope and compared normal ones (top) with those where Cyclin B1 is not working (bottom).
A cell cycle protein plays a crucial role in cell division and its location in the cell determines when cells start to divide, a new study has found.
When cells divide too early there is more room for mistakes when DNA is copied – for example, losing chromosomes or gaining extra copies, which can lead to cancer.
Knowing how normal cells regulate the timing of correct cell division could help find weaknesses in cancer – as many molecules that regulate the cell cycle protein, called Cyclin-B1, are overactive in cancer cells.
In the future, a better understanding of the role of Cyclin-B1 in the timing of cell division could lead to new ways of stopping cancer cell growth.
Scientists at The Institute of Cancer Research, London, worked with colleagues at the University of Cambridge to look at Cyclin-B1, a protein thought to be important in cancer cells but whose requirement for cell division had recently been questioned.
The study, published in the Journal of Cell Biology last month, was supported by the Wellcome Trust, the Medical Research Council and Cancer Research UK.
Essential for cell growth
The researchers designed a special set-up to study mouse embryos under a microscope from fertilisation onward, allowing them to visualise Cyclin-B1 in the very first cell divisions in early development.
They found that in embryos without the gene for Cyclin-B1, cells stopped growing after only two divisions, while cells with the gene continued to divide.
The first two divisions were possible because of remaining RNA from the egg cell – but when this ran out cells stopped growing, showing that the protein is necessary for cell division.
When they added Cyclin-B1 to cells without the gene, the team found that only a tiny amount was enough to trigger cell division – explaining why previous studies had found contradictory results.
Cellular location is important
The detailed time-lapse created under the microscope also allowed the researchers to look in close detail at why Cyclin-B1 moves in and out of the nucleus as cells prepare to divide.
They found that when the protein was kept away from the nucleus, cells did not divide at all – but that cell division happened too soon when it was locked inside the nucleus.
Having shown that Cyclin-B1 is necessary for cell division in very early mouse embryos, the researchers now plan to study Cyclin-B1 in human cancer cells and healthy cells.
Using a genome editing technique to switch genes on and off, they aim to further study the role of Cyclin-B1 and its export from the nucleus in the correct timing of cell division.
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Fundamental discoveries for future developments
Professor Jon Pines, Head of Cancer Biology at the ICR, said:
“In our study, we visualised the very first cell divisions in mouse embryos. We found that not only are cells unable to divide without Cyclin-B1, but that its location in the cell is carefully controlled and vitally important for the correct timing of cell division.
“Basic science where we explore the fundamental processes behind cancer is so important for future developments in cancer treatment. We could soon explore Cyclin-B1, and the network of molecules and proteins that regulate it, to find new ways of tackling cancer.”