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Tissue mechanical properties such as rigidity and fluidity, and changes inthese properties driven by jamming-unjamming transitions (UJT), have come underrecent highlight as mechanical markers of health and disease in variousbiological processes including cancer. However, most analysis of thesemechanical properties and UJT have sidestepped the effect of cellular death anddivision in these systems. Cellular apoptosis (programmed cell death) andmitosis (cell division) can drive significant changes in tissue properties. Thebalance between the two is crucial in maintaining tissue function, and animbalance between the two is seen in situations such as cancer progression,wound healing and necrosis. In this work we investigate the impact of celldeath and division on tissue mechanical properties, by incorporating specificmechanosensitive triggers of cell death and division based on the size andgeometry of the cell within in silico models of tissue dynamics. Specifically,we look at cell migration, tissue response to external stress, tissue extrusionpropensity and self-organization of different cell types within the tissue, asa 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 altertissue mechanics when compared to systems without these events, but that thechoice of triggers driving these cell death and division events also alter thepredicted tissue mechanics and overall system behavior.

Differences in cell death and division rules can alter tissue rigidity and fluidization