Biology Reference
In-Depth Information
anchor the cell and prevent any more forward motion. They therefore have to be destroyed.
The destruction of focal adhesions seems to require the protease calpain, without which cells
show dramatically reduced trailing edge detachment and strongly inhibited migration.
59
Calpain can cleave many constituents of focal adhesions, such as integrins (on the
cytoplasmic side),
60
ezrin,
61
talin
62
and FAK,
63
so is an obvious potential mediator of focal
adhesion release. What is not yet clear is how its activity is targeted to the adhesions at
the rear of the cell, which need to be released, rather than those at the front that are still
needed for cell advance.
KEY POI
NTS TO TAKE FORWARD INTO THE NEXT CH
APTERS
The above brief account of cell locomotion was not meant to be a comprehensive review of
cell locomotion, but rather to provide an overview of those parts of the cell migration nano-
machinery whose regulation has been shown to be key to morphogenetic events. The most
important points to take forward into the next chapter are:
Protrusion of the leading edge of the cell depends on Arp2/3-driven formation of
a branched actin network, and the balance of elongation and capping activity.
Arp2/3, and other aspects of the lamellipodium/filopodia, are controlled by the small
GTPases Rac and cdc42.
Integrin-mediated cell adhesion is key to crawling locomotion, and tensions generated
against the substrate through focal adhesions are used to move the bulk of the cell
forwards towards the lamellipodium.
Release of adhesion via the calpain and other systems is critical to continuous cell
movement.
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