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SUMMARY:Developing cell-scale biomimetic models involving lipid vesicles. 
 - Miglena Angelova\,  Université Pierre et Marie Curie\, Paris
DTSTART:20101112T140000Z
DTEND:20101112T150000Z
UID:TALK26614@talks.cam.ac.uk
CONTACT:Erika Eiser
DESCRIPTION:Vesicles are closed membranes of spherical shape separating a 
 water compartment from the bulk water. Cell-sized or giant unilamellar ves
 icles (GUV)\, 10 to 100 µm in diameter\, are quite efficiently prepared b
 y the liposome electroformation method. GUVs proved to be useful model for
  studying the role of membrane heterogeneity and compartmentalization in m
 embrane interactions as far as (i) GUVs composition can be precisely contr
 olled\; (ii) GUVs sizes permit direct optical microscopy observation of me
 mbrane dynamics – shape and morphology transformations. For example\,  w
 e developed  model membranes for considering the controversy regarding bio
 logical “rafts” (1). Recently (2) we have designed a minimal membrane 
 system (giant unilamellar vesicles\, GUV) mimicking mitochondrial inner me
 mbrane\, and\, we showed experimentally that the modulation of local pH gr
 adient at membrane level of cardiolipin-containing vesicles induces dynami
 c tubular membrane invaginations similar to mitochondrial cristae. Further
 more\, we have proposed a theoretical model (3) for elucidating the physic
 al background of a particular membrane instability - membrane tubule forma
 tion\, triggered by local pH modulation.\n\nIn this talk: An example of mo
 del membranes study related to the Alzheimer's disease and the molecular m
 echanisms of Amyloid  peptide (A) - induced neuronal cell death.\n	I
 t is recognized now that the AD progress leads to typical morphological an
 d functional pathological features regarding neurons at both the extracell
 ular (deposits of “plaques” – oligomers\, fibrils and amorphous aggr
 egates of A)\, and\, at the intracellular level (formation of “tangle
 s” – fibril aggregates of the microtubule-associated protein tau\; A
 -induced mitochondria dysfunctions). \nThe A-induced mitochondria dy
 sfunctions is the subject of our latest work (4). Using giant unilamellar 
 vesicles GUVs for modeling mitochondrial IM\, we could monitor directly th
 e real time macroscopic (vesicle scale) effects of A (1-42) on the lipi
 d membrane dynamics\, ultimately leading to the failure to form the crista
 e-like dynamic morphology.\n	The role of gangliosides in membrane heteroge
 neity and interactions related to extracellular deposits of “senile plaq
 ues” is the subject our forthcoming project\, which  I shall present at 
 the end of my talk.\n1. 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.\n2. Khalifat N\, Puff N\, Bonneau S\, F
 ournier J-B\, Angelova M I (2008) Biophys J  95 :4924-4933\, Membrane Defo
 rmation under Local pH Gradient: Mimicking Mitochondrial Cristae Dynamics.
 \n3. Fournier J-B\, Khalifat N\, Puff N\, Angelova M I (2009) Phys Rev Let
 t 102 : 018102-018104\, Chemically Triggered Ejection of Membrane Tubules 
 Controlled by Intermonolayer Friction.\n4. Khalifat N\, Puff  N\, Angelova
  MI (2009) in preparation\, The Amyloid-beta and the failure of mitochondr
 ial cristae dynamics. A study involving cell-sized vesicles.\n
LOCATION:Pippard Lecture Theatre\, Cavendish Laboratory
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