Stine Lauritzen Sønder

Suda and colleagues explore the enduring consequences of plasma membrane injury in budding yeast and mammalian cells. Their findings highlight that membrane damage induces irreversible cell-cycle arrest and premature cellular senescence, whereas upregulation of plasma membrane repair suppresses them.

Molecular dynamics simulations For molecular-level insight into how TFP-treated membranes affect ANXA2 binding and curvature induction, we performed all-atom molecular dynamics (MD) simulations of ANXA2 in proximity to a lipid bilayer, in the absence (Fig. 5) and presence of TFP in the membrane (Fig. 6). The interactions of ANXA2 protein with negatively charged phosphatidylserine lipids on the bilayer surface were mediated by Ca2+ ions (Fig. 5 and Video S5).

Abstract The plasma membrane shapes and protects the eukaryotic cell from its surroundings and is crucial for cell life. Although initial repair mechanisms to reseal injured membranes are well established, less is known about how cells restructure damaged membranes in the aftermath to restore homeostasis. Here, we show that cells respond to plasma membrane injury by activating proteins associated with macropinocytosis specifically at the damaged membrane.