Developing cell-scale biomimetic models involving lipid vesicles.

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• Miglena Angelova, Université Pierre et Marie Curie, Paris
• Friday 12 November 2010, 14:00-15:00
• Pippard Lecture Theatre, Cavendish Laboratory.

If you have a question about this talk, please contact Erika Eiser.

Vesicles are closed membranes of spherical shape separating a water compartment from the bulk water. Cell-sized or giant unilamellar vesicles (GUV), 10 to 100 µm in diameter, are quite efficiently prepared by the liposome electroformation method. GUVs proved to be useful model for studying the role of membrane heterogeneity and compartmentalization in membrane interactions as far as (i) GUVs composition can be precisely controlled; (ii) GUVs sizes permit direct optical microscopy observation of membrane dynamics – shape and morphology transformations. For example, we developed model membranes for considering the controversy regarding biological “rafts” (1). Recently (2) we have designed a minimal membrane system (giant unilamellar vesicles, GUV ) mimicking mitochondrial inner membrane, and, we showed experimentally that the modulation of local pH gradient at membrane level of cardiolipin-containing vesicles induces dynamic tubular membrane invaginations similar to mitochondrial cristae. Furthermore, we have proposed a theoretical model (3) for elucidating the physical background of a particular membrane instability – membrane tubule formation, triggered by local pH modulation.

In this talk: An example of model membranes study related to the Alzheimer’s disease and the molecular mechanisms of Amyloid  peptide (A) – induced neuronal cell death. It is recognized now that the AD progress leads to typical morphological and functional pathological features regarding neurons at both the extracellular (deposits of “plaques” – oligomers, fibrils and amorphous aggregates of A), and, at the intracellular level (formation of “tangles” – fibril aggregates of the microtubule-associated protein tau; A-induced mitochondria dysfunctions). The A-induced mitochondria dysfunctions is the subject of our latest work (4). Using giant unilamellar vesicles GUVs for modeling mitochondrial IM, we could monitor directly the real time macroscopic (vesicle scale) effects of A (1-42) on the lipid membrane dynamics, ultimately leading to the failure to form the cristae-like dynamic morphology. The role of gangliosides in membrane heterogeneity and interactions related to extracellular deposits of “senile plaques” is the subject our forthcoming project, which I shall present at the end of my talk. 1. Staneva G, Seigneuret M, Koumanov K, Trugnan G, Angelova MI (2005) Chem Phys Lip 136:55-66, Detergents induce raft-like domains budding and fission from giant unilamellar heterogeneous vesicles. A direct microscopy observation. 2. Khalifat N, Puff N, Bonneau S, Fournier J-B, Angelova M I (2008) Biophys J 95 :4924-4933, Membrane Deformation under Local pH Gradient: Mimicking Mitochondrial Cristae Dynamics. 3. Fournier J-B, Khalifat N, Puff N, Angelova M I (2009) Phys Rev Lett 102 : 018102-018104, Chemically Triggered Ejection of Membrane Tubules Controlled by Intermonolayer Friction. 4. Khalifat N, Puff N, Angelova MI (2009) in preparation, The Amyloid-beta and the failure of mitochondrial cristae dynamics. A study involving cell-sized vesicles.

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