Researchers from the Cell Cycle research group of the Institute of Biomedical Research of Bellvitge (IDIBELL), led by Dr. Ethel Queralt, have identified the mechanism that allows the polo-like protein kinase Cdc5 to regulate the last stages of mitosis, immediately before cell division. The results, published by Cell Reports, may suppose a crucial step towards developing specific and more direct anticancer therapies.
The proper development of mitosis, the process that occurs prior to cell division, is particularly important in order to maintain chromosomal stability. Defects in the separation or distribution of chromosomes can generate altered cells with too much or too little genetic material, which is something common in tumor cells. However, despite its importance, the regulatory mechanisms of this process are still very little known.
In this study, the research group describes a new mechanism of regulation of mitotic exit. To complete this process, a protein called Cdc14 must be activated, i.e. able to do its function; this is achieved through two regulatory mechanisms called FEAR (CdC fourteen early anaphase release) and MEN (Mitotic exit network). It was already known that another protein, polo-like kinase Cdc5, played an important role in this mechanisms, but the new article deals with the molecular mechanism by which this Cdc5 is also sequentially regulated by another protein called Cdk1.
In this study, as in most of those carried out by this research group, the Saccharomyces cerevisiae yeast (beer yeast) was used as a model organism. Yeast is one of the most widely used model organisms to study basic processes in the cell, allowing identification and description of complex molecular mechanisms, such as those related to the cell cycle, which would be impossible to study directly in higher organisms.
The application of the knowledge obtained through research in model organisms can potentially help develop more direct and effective cancer treatments. Quoting Dr. Queralt, "mitotic regulation mechanisms are very complex, but knowing them well at the molecular level will allow us to develop specific drugs that can inhibit or correct this process in various diseases, such as cancer, while minimizing side effects". Thus, the study by IDIBELL’s research group is an important step towards the development of therapies that prevent tumor cells from replicating.
Article citation:
Rodriguez-Rodriguez, et al.Mitotic Exit Function of Polo-like Kinase Cdc5 Is Dependent on Sequential Activation by Cdk1. Cell Reports 15, 1–13 (2016).
Image: Graphical Abstract
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