  Tissue mechanical properties such as rigidity and fluidity, and changes in
these properties driven by jamming-unjamming transitions (UJT), have come under
recent highlight as mechanical markers of health and disease in various
biological processes including cancer. However, most analysis of these
mechanical properties and UJT have sidestepped the effect of cellular death and
division in these systems. Cellular apoptosis (programmed cell death) and
mitosis (cell division) can drive significant changes in tissue properties. The
balance between the two is crucial in maintaining tissue function, and an
imbalance between the two is seen in situations such as cancer progression,
wound healing and necrosis. In this work we investigate the impact of cell
death and division on tissue mechanical properties, by incorporating specific
mechanosensitive triggers of cell death and division based on the size and
geometry of the cell within in silico models of tissue dynamics. Specifically,
we look at cell migration, tissue response to external stress, tissue extrusion
propensity and self-organization of different cell types within the tissue, as
a function of cell death and division and the rules that trigger these events.
We find that not only do cell death and division events significantly alter
tissue mechanics when compared to systems without these events, but that the
choice of triggers driving these cell death and division events also alter the
predicted tissue mechanics and overall system behavior.
