A systems biology approach to study the role and evolution of molecular pathways related to multicellularity
Human body is composed of cells that are complex molecular machines. These machines are not infallible and due to external agents or internal error, they can start to function in an undesired manner. An example of such malfunction is the disruption of cell division mechanism that leads to its uncontrolled reproduction. To prevent such a multiplication, cells are equipped with a programmed cell death (PCD) mechanism. This system triggers the “self-destruction” of an affected cell in a way that does not pose a threat to neighboring cells. Unfortunately, sometimes the PCD failsafe mechanism may be also damaged, and in this case, the cell will keep on multiplying in an unrestrained manner – a condition that we know as cancer.
Previous studies indicated that neither cancer nor PCD processes are unique to humans. On the contrary, both are observed in a variety of multicellular organisms including starfish, freshwater polyp, and fungi. Moreover, it has been shown that the molecular circuits (i.e., group of proteins acting together) responsible for PCD are also present in bacteria characterized by a complex lifestyle, suggesting that the ancestors of the PCD systems appeared very early in the history of life.
In this project, we use computational biology tools to identify, characterize, and classify the individual components of PCD and PCD-like systems across thousands of the available sequenced genomes. These analyses will enable us to understand the differences in the composition of PCD systems originating from various organisms and to describe the evolutionary processes underlying this diversity. The computational analyses will allow us to formulate experimentally verifiable hypotheses about PCD function and evolution. In particular, we are interested in studying the compatibility between PCD components from different species and discovering the factors that cause their activation in bacterial cells.