University of Dundee researchers discover the process of cell division that was commonly believed is wrong – Health News Scotland

Researchers from the University of Dundee have discovered how a cellular “traffic light controller” helps protect against the DNA damage that can lead to cancer.

Dr  Adrian Saurin and his colleagues from the University’s School of Medicine found that the process of cell division does not work in the way that was commonly believed.

The team investigated enzymes known to be vital to cell division. The process in which a parent cell divides into two daughter cells containing the same DNA content.

If this process goes wrong, and the DNA is not partitioned equally, then diseases such as cancer can arise.

To safeguard against these errors, the cell uses two classes of enzymes, known as kinases and phosphatases, to monitor division.

The discovery could potentially allow scientists to understand how cells divide with errors in cancer.

Dr Saurin said: “Kinases and phosphatases control a traffic signal that tells cells whether it’s safe to divide or not. If this goes wrong then cells can crash and damage their DNA in ways that could lead to cancer.

“It was previously assumed that the kinases put the signal on red and then, when it is safe, the phosphatases wipe that signal out and turn it green again. What we found is that it doesn’t work quite like that. The main role of the phosphatases was not to turn signals green but to stop the kinase from working altogether.

“So a better analogy is that the phosphatase pulls the plug to turn the lights out when the time is right. This is important because it may allow us to appreciate how errors occur during cell division in cancer cells. This may also be a common feature of how our cells work, since many processes rely on similar stop/go signals.”

The researchers will now look to work out whether cancer cells hijack aspects of this process to override the traffic light system and produce the type of division errors that fuel tumour evolution.

The research was funded by Cancer Research UK and is published in the latest edition of the Journal of Cell Biology.