Supplementary material from "The mechanobiology of actin cytoskeletal proteins during the cell–cell fusion"

Myosin II and spectrin β displayed mechanosensitive accumulations in the invasive protrusions during the cell–cell fusion of Drosophila myoblasts. The biochemical inhibition and deactivation of these proteins resulted in significant fusion defects. Yet, a quantitative understanding of how the protrusion geometry and fusion process are linked to these proteins is still lacking. Here we present a quantitative model to interpret the dependence of the protrusion size and the protrusive force on the mechanical properties and microstructures of the actin cytoskeleton and plasma membrane based on a mean-field theory. We build a quantitative linkage between the mechanosensitive accumulation of myosin II and the fusion pore formation at the tip of the invasive protrusion through the local area dilation. The mechanical feedback loop between myosin II and local deformation suggests that myosin II accumulation possibly reduces the energy barrier and critical radius of fusion pore. We also analyse the effect of spectrin β on maintaining the proper geometry of the protrusions required for the success of the cell–cell fusion.