Protocols Freezer NoteBook Bibliography Parts WetLab DryLab

Team Collaborations Contacts Acknowledgements Links

DryLab

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.

• 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 [] 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 and so the local deformation of the outer membrane.

Defects in the TOL-PAL system leads to vesicles maturation. 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. Using those type 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 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 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.