A team of scientists at UmeĆ„ University in Sweden found that the movement of a protein complex known as the Mediator along DNA genes could influence cell division. This breakthrough could have significant implications for future medical research and potential treatments for various diseases.”Understanding the causes of diseases related to cell division errors, such as tumors, is crucial,” said Stefan Bjƶrklund, a professor at UmeĆ„ University’s Department of Medical Biochemistry and Biophysics and the study’s lead author.
Within each cell, there is a machinery known as “the ribosome” that uses DNA to create proteins essential for various cell processes. Before this, cells must create a copy of the instructions in the form of mRNA, a process known as transcription.
The research team at UmeĆ„ University has identified how theMediator, a protein complex located in the cell nucleus, has the ability to bind to DNA and interact with another protein complex known as Lsm1-7 in order to regulate the production of proteins that are essential for the formation of ribosomes. The research indicates that when cells become too crowded, the process of cell division is hindered. In this situation, the mediator relocates to the end of the genes and interacts with Lsm1-7. This results in the dual effect of slowing down the genes’ reading process and disrupting the mRNA maturation. As a result, there is a decrease in the production of ribosomal proteins, which ultimately leads to a slower cell division.
A potential avenue for future research could involve examining the impact of this interaction on cell function.This article explores the potential for controlling the position of the mediator to slow down cell division in conditions such as tumors. Stefan Bjƶrklund states that while more research is needed to confirm the viability of this approach, it presents an exciting opportunity. The study focused on yeast cells as a model for understanding fundamental mechanisms that are relevant to more complex systems like animal and plant cells.