Role of Atypical Cyclins in the control of cell cycle

The scientific community has broadly accepted the key role of the complex formed by cyclins and CDKs. Nevertheless, it exists a broad variety of cyclins and CDKs with apparently redundant function. The importance and the role of this redundancy are not understood in the physiology of a living cell, especially when the elimination of some of them produces a non-evident phenotype.

Saccharomyces cerevisiae controls G1 progression by means of two different families of cyclins (Cln and Pcl families) and two CDK’s (Cdc28 and Pho85). We want to answer the question of the functional redundancy of the different CDK’s complexes controlling G1. Using S. cerevisiae as a model, we want to demonstrate that Pcl/Pho85 complex has specific substrates, regulates specific functions and is differently regulated to the other cyclin/CDK complex (Cln/Cdc28) in eukaryotic cells. We want to uncover the physiological relevance of the Pcl/Pho85 complexes in non-standard lab conditions expecting an essential role in such more “real” environments. We also want to demonstrate that some of the substrates and regulatory functions of the CDK/Pcl complex are evolutionary conserved in human cells. In this context, it must be noted that the human genome sequence project has unveiled the presence of a whole plethora of new cyclins with unknown functions, showing structural differences with the canonical ones but, surprisingly, very similar to the yeast Pcls. We have obtained results supporting the idea that the newly discovered Pcl-like cyclins are responsible for carrying out some new important functions during G1 phase in both yeast and human cells. Our efforts are focused to know more about the role of this new cyclins.

As a consequence of the fluent colaboration with the Martí Aldea’s group at IRB we are contributing to Aldea’s question regarding the regulation of cell size by CDK-cyclin complexes.