Abstract
Plasma membrane tension is responsible for a variety of cellular functions such as motility, cell division, and endocytosis. Since membrane tension is dominated by the attachment of the actin cortex to the inner leaflet of the plasma membrane, we investigated the importance of ezrin, a major cross-linker of the membrane-cytoskeleton interface, for cellular mechanics of confluent MDCK II cells. For this purpose, we carried out ezrin depletion experiments and also enhanced the number of active ezrin molecules at the interface. Mechanical properties were assessed by force indentation experiments followed by membrane tether extraction. PIP2 micelles were injected into individual living cells to reinforce the linkage between plasma membrane and actin-cortex, while weakening of this connection was reached by ezrin siRNA and administration of the inhibitors neomycin and NSC 668394, respectively. We observed substantial stiffening of cells and an increase in membrane tension after addition of PIP2 micelles. In contrast, reduction of active ezrin led to a decrease of membrane tension accompanied by loss of excess surface area, increase in cortical tension, remodelling of actin cytoskeleton, and reduction of cell height. The data confirm the importance of the ezrin-mediated connection between plasma membrane and cortex for cellular mechanics and cell morphology.
Highlights
Other factors affecting plasma membrane tension include hydrostatic pressure across the membrane, and effects due to local membrane curvature associated with microvilli or invaginations such as caveolae[21]
Tether pulling of PIP2-microinjected MDCK II cells in comparison to untreated cells revealed that membrane tension is mainly governed by the presence of active ezrin[17]
This finding was urging the question to what extent this membrane-cortex interface is responsible for the mechanical properties of living epithelial cells and how tension is used by epithelial cells for mechanotransduction
Summary
Other factors affecting plasma membrane tension include hydrostatic pressure across the membrane, and effects due to local membrane curvature associated with microvilli or invaginations such as caveolae[21]. Even lower tension is only found if the cytoskeleton is compromised or phosphatidylinositol 4,5-bisphosphate (PIP2) is depleted from the plasma membrane[16] This implies that mammalian cells use membrane-remodeling mechanisms to buffer tension changes such as endocytosis and exocytosis and release of membrane material from reservoirs in the plasma www.nature.com/scientificreports/. Tension-driven surface area regulation is realised through supply of excess plasma membrane area to accommodate high tension and a reduction of membrane area if the tension is low Along these lines, Nassoy and coworkers reported that cells respond to mechanical stress by sacrificing caveolae structures compensating an increase in tension[28]. Regardless of how ezrin is removed from the membrane-cortex interface, membrane tension decreases, cells sacrifice excess surface area, and cells contract
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
