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Team:Paris/Modeling
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DryLab
Introduction
Vesicles Maturation Modeling.
- This part of the modelling works was dedicated to the vesicles creation understanding. Indeed if we want to control the emission of vesicles we need to discuss phenomenon which lead it. We decided to attach ourselves to the biophysics of the problem and especially on the biophysics of membranes. We finally linked the creation of vesicles to the free diffusion of PAL and TOL proteins in the membranes depending of the lipidic bilayer shapes.
- We demonstrate that two simple physical phenomenon and the Tol/pal binding can explain the creation of vesicles:
Osmotic pressure increase due to the Cell Wall turnover and the Tol/Pal distinct location can explain the formation of blebbing
- the hypothesis made in Reference about a link between vesicles creation and the turnover of the peptidoglycan act as a physical motor for our model : Indeed during the division of the cell, the peptidoglycan is degraded and reconstructed to be given a new shape. This turnover isn’t perfect: a part of the murrains components are released in the periplasm which make locally increased the pressure and so cause the local deformation of the outer membrane.
- Defects in the TOL-PAL system leads to vesicles maturation reference. We can consider that TOL-PAL is acting as mooring ropes. So the distribution of TOL-PAL in the lipidic bilayer would be vital for the integrity of the outer membrane of the bacteria and any defect in those distributions can lead to vesicle maturation if there is any increase of the periplasm pressure. During vesicle creation Tol-Pal system act as counter forces to the osmotic pressure increase unabling a global swelling of the outer membrane. Using those types of information we create a 2 dimension model to explain the formation of blebbing
Brownian diffusion in the membranes can explains the affinity for concave region of outer membrane in bacteria and local clustering on the border of blebbing.
- Our hypothesis to this model is that simple Brownian diffusion on the surface can explain stable accumulation of TOL and PAL in the border of the blebbing ( Link toward Details). Indeed physically it appears that Brownian motion model on a non-plane surface doesn’t predict a non uniform concentration of particles. They will aggregate themselves in the highly concave areas of membranes. This prediction is in agreement with some observation about Tol/Pal Reference and some experiments were done which confirm a phenomena in Reference which is the accumulation of proteins in the septa region during E.coli division but not explained efficiently by simple biology mechanism.
Brownian Diffusion predict accumulation of TOL-PAL on the border of vesicles in creation phases.
- During the osmotic pressure increase if the TOL-PAL proteins complexes are not enough to create a tight net, blebbings can appear. On their border the curvature is negative and will be quickly populated by free PAL they will tend to attach themselves to the TOL complex localized in the inner membrane behind the cell wall and so the border of the blebbing is tightening itself. If the bleb is important enough the negative spontaneous curvature of the lipid bilayer of E.Coli ensures the tightening of the border would not retract the whole blebbing but just the border between the blebbing and the outer membrane. this end the maturation of the blebbing in a vesicle.
