Biomedical Engineering Reference
In-Depth Information
Figure 2.7.
Traction force measurements in keratocytes. (a) Phase contrast image
of a keratocyte moving (in the direction indicated by the large arrow) on a silicone
rubber substratum with embedded beads. The cell is outlined in white for clarity.
(b) Traction map for the same cell. Each small arrow represents the magnitude and
direction of the traction stress at the location corresponding to the tail of the arrow.
Reproduced and modified from [41]. Copyright (1999) permission of The Rockefeller
University Press.
and the fact that myosin clusters remain stationary with respect to the actin
cytoskeleton, indicate that direct transport by myosin moving along actin
tracks as a mechanism for pulling the cell body is not a plausible model.
Another model [37] suggests that the cell body moves forward by rolling, which
results from tension generated by myosin contraction along the actin bundles
at the rear of the cell. While rolling of the cell body is observed in moving
cells [37], its magnitude varies between different cells and, in most cases, is not
sucient to account for all the forward translocation of the cell body [38]. Yet
another model [38] suggests that contraction of the actin-myosin cytoskeleton
at the transition zone between the lamellipodium and the cell body induces
forward translocation of the cell body.
While it is obvious that myosin contraction in keratocytes leads to reori-
entation of the actin network in the transition zone between the cell body
and the lamellipodium [38] and is responsible for the observed inward flow of
actin at the rear of the cell, the importance of these processes for steady state
motility is not clear. Experiments in which myosin II activity was eliminated
either by specific drugs or by deletion indicate that myosin II is not essential
for steady state motility. For example, keratocytes treated with blebbistatin,
a specific inhibitor of myosin II, continue to move although with reduced per-
