Figure 6

Consequences of altered reaction rates and apoptosome immobilisation on spatial anisotropies during apoptosis execution. (A, B) Acceleration of biochemical reactions promotes maintenance of spatial anisotropies during apoptosis execution. (A) The end-to-end delays in onset of substrate cleavage (1%) as well as the delays for half maximal substrate cleavage by effector caspases were calculated for a 10-fold increase in biochemical reaction rates. In parallel, diffusivity was modified across 5 orders of magnitude. (B) End-to-end delays from the non-perturbed reference model were subtracted from the results displayed in (A). Positive values represent an increase in spatial anisotropy. (C, D) Immobilized apoptosomes promote spatial anisotropies during apoptosis execution. (C) Assuming immobile apoptosome complexes, the end-to-end delays in onset of substrate cleavage (1%) as well as the delays for half maximal substrate cleavage by effector caspases were calculated. In parallel, diffusivity was modified across 5 orders of magnitude. (D) End-to-end delays from the non-perturbed reference model were subtracted from the results displayed in (C). Positive values represent an increase in spatial anisotropy. (E, F) Influence of a combination of accelerated biochemical reactions and macromolecule immobilisation on spatial anisotropies during apoptosis execution. (E) The end-to-end delays in onset of substrate cleavage (1%) as well as the delays for half maximal substrate cleavage by effector caspases were calculated. In parallel, diffusivity was modified across 5 orders of magnitude. (F) End-to-end delays from the non-perturbed reference model were subtracted from the results displayed in (E). Positive values represent an increase in spatial anisotropy.