Thursday 14 November 2019, 1.00PM
Speaker(s): Maria Rosa Domingo-Sananes, University of Nottingham
The eukaryotic cell cycle control system is based on the activity of cyclin-dependent kinases (CDKs) and many additional proteins that regulate progress through the cycle and relay signals from multiple checkpoints. Given the fundamental role of this system, it is expected that the basic control network should be highly conserved across eukaryotes. However, most of our current knowledge about cell cycle control derives from a few species of animals and fungi, which we now know poorly represent eukaryotic diversity. Furthermore, recent analyses suggest that cell cycle control may differ significantly across the eukaryotic tree of life. For example, the malaria parasite Plasmodium divides without classical mitotic cyclins and the gut parasite Giardia lacks the Anaphase Promoting Complex (APC). Taking advantage of the increasing availability of whole genome sequences from diverse eukaryotes, we have performed phylogenetic analyses to survey the distribution of more than 30 cell cycle-associated proteins. The phylogenetic patterns of these proteins vary substantially in the analysed genomes and we find only a small set of ‘core’ proteins, including Aurora-like kinases and PPA2 phosphatases, present in most organisms. Surprisingly, many proteins with key roles in animals/fungi are not detected in some or all representatives of specific eukaryotic lineages. This includes important proteins such as Cdc2 and type-B cyclins, highlighting major differences in the repertoire of regulators among eukaryotes. Therefore, cell cycle control appears to change rapidly on evolutionary time scales and is highly diverse. Furthermore, our analysis suggests that last eukaryotic common ancestor (LECA) already had a complex cell cycle control machinery. This has important implications for understanding the origins, evolution and function of the cell cycle control system. Many questions remain about how most eukaryotes, including important pathogens, control cell cycle progression and the reasons behind this unexpected diversity.
Location: Dianna Bowles Lecture Theatre B/K/018