Actin self-assembly, cell crawling and Listeria motility

by: Andrea J. Liu

Abstract

Actin self-assembly, cell crawling and Listeria motility
When a cells crawls, its shape re-organizes via polymerization and
depolymerization of a network of actin filaments.� The growing ends
of the filaments are localized near the outside of the cell, and
their polymerization, regulated by a host of proteins, pushes the
cell membrane forwards in a biological model known as the dendritic
nucleation model.� We have developed a formulation of this model that
allows study of the morphology of actin networks, and find that it
yields results in quantitative agreement with simulations and
experiments.� The same dendritic nucleation mechanism comes into play
when the bacterial pathogen Listeria monocytogenes infects a cell.�
The bacterium hijacks the host cell's actin machinery to create an
actin network (the actin comet tail) that propels the bacterium
through cells and into neighboring cells.� We propose a new mechanism
for how polymerization gives rise to motility.� We treat the actin
comet tail as an elastic continuum tethered to the rear of the
bacterium and calculate the inhomogeneous stresses that arise from
the interplay of polymerization and tethering with a finite element
analysis.� We quantitatively reproduce distinctive features of actin
propulsion that have been observed experimentally.��This work was
supported by NSF-DMR-0503347 and�NSF-CHE-0096492.