Mechanics and self-assembly in cancer cell nuclei
Fluids and Materials Seminar
14th February 2019, 2:00 pm – 3:00 pm
Main Maths Building, SM3
When cells migrate through constricting pores, there is an increase in DNA damage and mutations. Experimental observations show that this breakage is not due to mechanical stress. I present an elastic-fluid model of the cell nucleus, coupled to kinetics of DNA breakage and repair proposing a mechanism by which nuclear deformation can lead to DNA damage. I show that segregation of soluble repair factors from the chromatin during migration leads to a decrease in the repair rate and an accumulation of damage that is sufficient to account for the extent of DNA damage observed experimentally.
In the second part I will talk about how some types of cancer cells grow uncontrollably. Telomeres are DNA caps on the end of chromosomes and are shortened during each cell division. Tumour cells elongate their telomeres so that unlike healthy cells they do not undergo programmed death. I will show how some types of cancer cells can control microphase separation to form micelle-like structures with telomeres in the cores. This clustering of telomeres is a crucial step in the elongation process and understanding the physics involved can help us understand how this process could be disrupted.