Actin polymerization provides the force that directly drives cell motility in a large number of situations, but some observations suggest that amoeboid motions might rely on distinct mechanisms. Using the model of Entamoeba histolytica, we previously observed that these cells produce transient protrusions that are necessary for cell motions. Mutations affecting myosin activity and adhesion molecules inhibit the protrusive activity and cell motility (Coudrier et al, Cell Microbiol. 2005). Following on these observations, we postulated that ameboid motions of Entamoeba histolytica are controlled by a cyclic dynamic instability of the cell cortex: the plasma membrane produces a bleb by unbinding from the cortical cytoskeleton under the action of the internal pressure generated by acto-myosin contraction, and the actin cortex reassembles at the surface of the blebs. The fast initial expansion (faster than actin polymerization) and the analogy with apoptotic blebs produced by the proteolytic disruption of cytoskeleton-membrane links, was a strong indication that Entamoeba histolytica moves by projecting initially cytoskeleton-free blebs, which is confirmed by live fluorescence microscopy of stained F-actin. Experimentally, the protrusion formation has been analyzed in details by video-microscopy. Protrusions first expand during a few hundreds of milliseconds with very high velocities (up to a few tens of μm/s). Then, expansion goes on with locally spherical membrane shape and no intracellular vesicles. At a later stage, the actin cortex collapses and further expansion appears to be powered by a larger flow with intracellular vesicles. Alternatively, protrusions can retract or get stabilized. The blebbing / stabilization cycle leads to random net cell motions sustained over hours. We present here a physical model that describes the control parameters of the dynamic instability. Using suction pressure of a micropipette, we are able to trigger protrusions, and controled geometry of the experiment gives rise to reproducible protrusive events, pretty well decribed by theoretical models. Such cortical instabilities may thus represent a distinct to generate cell motility, relevant for pathogen invasion and immune cell motions.

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   |wiki=    Wicri/Psychologie
   |area=    BernheimV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     Hal:tel-00512834
   |texte=   A membrane unbinding transition drives cortical dynamics instabilities and cell motility
}}