Cells are wrapped in inelastic membranes, yet they can sustain large mechanical strains by regulating their area. The area regulation in cells is achieved either by membrane folding or by membrane exo- and endocytosis. These processes involve complex morphological transformations of the cell membrane, i.e., invagination, vesicle fusion, and fission, whose precise mechanisms are still under debate. Here we provide mechanistic insights into the area regulation of cell membranes, based on the previously neglected role of membrane confinement, as well as on the strain-induced membrane tension. Commonly, the membranes of mammalian and plant cells are not isolated, but rather they are adhered to an extracellular matrix, the cytoskeleton, and to other cell membranes. Using a lipid bilayer, coupled to an elastic sheet, we are able to demonstrate that, upon straining, the confined membrane is able to regulate passively its area. In particular, by stretching the elastic support, the bilayer laterally expands without rupture by fusing adhered lipid vesicles; upon compression, lipid tubes grow out of the membrane plane, thus reducing its area. These transformations are reversible, as we show using cycles of expansion and compression, and closely reproduce membrane processes found in cells during area regulation. Moreover, we demonstrate a new mechanism for the formation of lipid tubes in cells, which is driven by the membrane lateral compression and may therefore explain the various membrane tubules observed in shrinking cells.

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In March 2014 a group of early career researchers and academics from São Paulo state and from the UK met at the University of Campinas to participate in a workshop on 'Responsible

. (2013) Reprinted with permission from the American Physical Society: Phys. Rev. Lett. 110, 028101 c (2013) by the American Physical Society. Readers may view, browse, and/or download material for temporary copying purposes only, provided these uses are for noncommercial personal purposes. Except as provided by law, this material may not be further reproduced, distributed, transmitted, modi ed, adapted, performed, displayed, published, or sold in whole or part, without prior written permission from the American Physical Society. Additional information:Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-pro t purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details.

Electric pulses applied to fluid phospholipid vesicles deform them and can induce the formation of pores, which reseal after the end of the pulse. The mechanical and rheological properties of membranes in the gel phase differ significantly from those of fluid membranes, thus a difference in the vesicle behavior in electric fields is expected. However, studies addressing this problem are scarce. Here, we investigate the response of giant gel-phase vesicles to electric pulses and resolve the dynamics of deformation with microsecond resolution. We find that the critical transmembrane potential leading to poration is several times higher as compared to that of fluid membranes. In addition, the resealing of the pores is arrested. Interestingly, the vesicle shapes change from ellipsoidal to spherocylindrical during the electric pulse and the membrane becomes periodically wrinkled with ridges aligned with the field direction and wavelengths in the micrometre range. Such membrane wrinkling has not been reported previously. The corrugations comply with universal laws of wrinkling of surfaces with lengthscale dimensions from nanometres to metres.