DOI: 10.1101/509182Jan 2, 2019Paper

Mammalian Amoeboid Swimming is propelled by molecular and not protrusion-based paddling in Lymphocytes

BioRxiv : the Preprint Server for Biology
Laurene AounOlivier Theodoly

Abstract

Mammalian cells developed two main migration modes. The slow mesenchymatous mode, like fibroblasts crawling, relies on maturation of adhesion complexes and actin fiber traction, while the fast amoeboid mode, observed exclusively for leukocytes and cancer cells, is characterized by weak adhesion, highly dynamic cell shapes, and ubiquitous motility on 2D and in 3D solid matrix. In both cases, interactions with the substrate by adhesion or friction are widely accepted as a prerequisite for mammalian cell motility, which precludes swimming. We show here experimentally and computationally that leukocytes do swim, and that propulsion is not fueled by waves of cell deformation but by a rearward and inhomogeneous treadmilling of the cell envelope. We model the propulsion as a molecular paddling by transmembrane proteins linked to and advected by the actin cortex, whereas freely diffusing transmembrane proteins hinder swimming. This mechanism explains that swimming is five times slower than the cortex retrograde flow. Resultantly the ubiquitous ability of mammalian amoeboid cells to migrate in various environments can be explained for lymphocytes by a single machinery of envelope treadmilling.

Related Concepts

Actins
Tissue Adhesions
Cell Motility
Cerebral Cortex
Environment
Fibroblasts
Integral Membrane Proteins
Leukocytes
Lymphocyte
Adheseal

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