Stress-triggered cell elimination stabilizes resource-limited cell collectives: An agent-based model

Mitochondria, long regarded as the cell's "powerhouses", also serve as intracellular quality-control modules that promote the elimination of damaged or proliferatively dysregulated cells. Alongside their energetic benefits, mitochondrial apoptosis regulation may have helped shape the earliest steps toward stable multicellular organization. An agent-based modeling framework is developed to isolate and quantify the evolutionary impact of a mitochondrial death-surveillance system under nutrient stress, independently of its energetic contribution. The model tracks two cell types - normal prokaryotic cells (NPCs) and dysfunctional prokaryotic cells (DPCs) - each characterized by three dynamic state variables: damage load, proliferation drive and energy deficit. Mitochondrial surveillance is formalized as a simplified rule that detects stress and eliminates dysfunctional cells when a critical dysregulation boundary is crossed. Across 1200 stochastic simulations spanning variable nutrient regimes and inoculum sizes, mitochondrial surveillance prolonged median colony-collapse time by approximately 17%-18% across both nutrient regimes. The results indicate that a mitochondria-linked, intrinsic apoptosis-like gate can stabilize simple microbial groups independently of bioenergetic benefit, and is consistent with the view that such quality-control mechanisms provided a selective advantage toward robust multicellular organization. The framework also provides a conceptual basis for viewing mitochondrial transplantation as a means to restore intracellular fate-decision control, rather than solely to augment energy supply, in settings such as aging and cancer.