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Team:Paris/Modeling
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iGEM > Paris > Home > DryLab > Modeling Introduction
Introduction
Et un petit blabla d'intro sur les modélisations, ho que oui vous adorez ca .. Ca sent bon le blabla :d
Non, ce n'est pas du blabla du tout. La raison pour laquelle vous avez passé tant de temps à faire de la modélisation n'est pas du tout accessoire. Fondamentale comme accompagnement à la réflexion sur le design du système et pour apprendre sur les mécanismes en jeu. Le travail de Piierre n'est peut être pasà ce stade immédiatement exploitable pour le projet, mais dans un perspective long terme une telle étude des mpécanismes biophysiques outre sont intérêt fondamental peut amener a des progrès importants pour les applicatiojns.
Vesicles Maturation Modeling.
(or how biophysic is important for the understanding of biological phenomenom ;)).
- 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:
- Brownian diffusion in the membranes can explains the affinity for concave region of outer membrane in bacteria.
- Our hypothesis to this model is that simple Brownian diffusion on the surface can explain stable accumulation of TOL and PAL in this area. Indeed physically it appears that Brownian motion model on a non-plane surface doesn’t predict a uniform concentration of particles. They will aggregate themselves in the highly concave areas of membrane. This prediction is in agreement with some observation about Tol/Pal Reference and some experiments were done which confirm a phenomena in [1] which is the accumulation of Pal in the septa region during E.coli division but not explained efficiently by simple biology mechanism.
- Defects in the TOL-PAL system leads to vesicles maturation. We can consider that TOL-PAL is acting as mooring ropes. The distribution of TOL-PAL in the membranes would so 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 an increase of the periplasm pressure.
- Thus we can here begin to speak about the hypothesis made in [] for a physical “motor” to our model: the Turgor pressure augmentation due to the cell wall turnover: Indeed during the division period 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.
- In normal condition the accumulation of porins in the septa during the division would be efficient enough to ensure the evacuation of molecules toward the medium and unable a wild local increase of pressure in the periplasm which would be not controlled by the mooring ropes system. But in stress condition TOL-PAL system is too weak to absorb this pressure increase and vesicle can mature during division.
- 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.
