The story is a synthesis of Villu Päärt’s article in Novaator and Ott Tammik’s coverage in the ERR News.
University of Tartu researchers have made new discoveries in the cell division cycle, which is one of life’s fundamental processes. This knowledge is essential in developing a more efficient treatment for cancer.
We all know that cells divide constantly. Cell division consists of a sequence of different complicated processes wherein exact copies of existing cells emerge. The protein CDK is “in charge” of keeping these processes on track.
The research team led by biomedical technology researcher Mart Loog discovered that the protein CDK regulates the complicated cell division process sort of like an on/off switch and acts as a trigger that changes at different times during the process.
“We discovered that CDK’s ability to give signals to various molecules changes constantly during the cell cycle and is not stable, as was long believed,” said Loog. “Hence we created a model that describes the changes of those signals during the cell division cycle. We also put together the first system to classify those signals, which is based on the yeast cell model.”
In cancer cells, the function of CDK protein is interrupted by a genetic mutation, and cellular division spirals out of control. It can be thought of as a switch that doesn’t want to turn off.
Studying how the CDK protein acts in cancer cases may be the key to learning how to interrupt a cell division process gone bad while avoiding damage to healthy cells. “To turn the switch off, we must understand the inner mechanism,” said Loog.
The process of cell division in humans and yeast is very similar. However, researchers still need to confirm that the discovered switch mechanism fully applies to humans.
The study is part of Mardo Kõivomägi’s doctoral thesis and was published in the journal Molecular Cell.
Kõivomägi M, Valk E, Venta R, Iofik A, Lepiku M, Morgan DO, & Loog M (2011). Dynamics of Cdk1 Substrate Specificity during the Cell Cycle. Molecular cell, 42 (5), 610-23 PMID: 21658602
