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Single Giant Vesicle Rupture Events Reveal Multiple Mechanisms of Glass-Supported Bilayer Formation

Chiho Hamai ^*, Paul S. Cremer  and Siegfried M. Musser ^*

^* Department of Molecular and Cellular Medicine, The Texas A&M University System Health Science Center, College Station, Texas; and Department of Chemistry, Texas A&M University, College Station, Texas

Correspondence: Address reprint requests to Siegfried M. Musser, Dept. of Molecular and Cellular Medicine, Texas A&M University Health Science Ctr., College Station, TX 77843. Tel.: 979-862-4128; Fax: 979-847-9481; E-mail: smusser{at}tamu.edu.

The formation of supported lipid bilayers (SLBs) on glass from giant unilamellar vesicles (GUVs) was studied using fluorescence microscopy. We show that GUV rupture occurs by at least four mechanisms, including 1), spontaneous rupture of isolated GUVs yielding almost heart-shaped bilayer patches (asymmetric rupture); 2), spontaneous rupture of isolated GUVs yielding circular bilayer patches (symmetric rupture); 3), induced rupture of an incoming vesicle when it contacts a planar bilayer edge; and 4), induced rupture of an adsorbed GUV when a nearby GUV spontaneously ruptures. In pathway 1, the dominant rupture pathway for isolated GUVs, GUVs deformed upon adsorption to the glass surface, and planar bilayer patch formation was initiated by rupture pore formation near the rim of the glass-bilayer interface. Expanding rupture pores led to planar bilayer formation in 10–20 ms. Rupture probability per unit time depended on the average intrinsic curvature of the component lipids. The membrane leaflet adsorbed to the glass surface in planar bilayer patches originated from the outer leaflet of GUVs. Pathway 2 was rarely observed. We surmise that SLB formation is predominantly initiated by pathway 1 rupture events, and that rupture events occurring by pathways 3 and 4 dominate during later stages of SLB formation.