Biomedical Engineering Reference
In-Depth Information
PlexinA1 to mediate repulsion by Sema 1a. PTK7 also interacts with
PlexinA1 to regulate cranial neural crest migration in
Xenopus
(
Wagner et al., 2010
). In chick, KLG/Otk is a coreceptor with PlexinA1
and VEGFR2 to respond to Sema6D in cell migration (
Toyofuku et al.,
2004
). These studies suggest that Semaphorin signaling may access this
machinery via PTK7 through the PCP side (
Fig. 6.5C
).
3
. N-Cadherin is long known to be a potent stimulator for axon out-
growth. N-Cadherin was found in the adherens junction of chick cardiac
muscle cells and lens epithelial cells and therefore can exert similar adhe-
sion and cell polarization functions as E-cadherin (
Volk & Geiger, 1984,
1986
). Recent studies show that a classic guidance system, Slit-Robo
system, can inhibit adhesion by both E-cadherins and N-cadherins
and regulate retinal neurite outgrowth, adhesion, or retinal ganglion
cell apical process retraction (
Rhee et al., 2007, 2002; Santiago-
Martinez et al., 2008; Wong et al., 2012
). Cadherin can interact with
aPKC and regulate its function (
Seifert et al., 2009
). Therefore, Slit
may access the cell polarity-based steering machinery via the cadherin
complex, which may affect both A-BP and PCP signaling (
Etienne-
Manneville, 2011
)(
Fig. 6.5C
).
4
. In addition to adherens junction, focal adhesion can also affect aPKC
(
Itoh et al., 2010
). Therefore, axon guidance signaling which affects focal
adhesion kinase may also access this cell polarity-signaling-based turning
machinery.
Therefore, it is possible that growth cone signaling can be unified under a
common cell polarity-based machinery. If this is true, this common cell
polarity-based compass in growth cone is analogous to the core cell cycle
mechanism (CDKs and cyclins), which controls cell cycle of all cell types
but can be regulated by many different factors and at different checkpoints
in different cell types.
9. SUMMARY
It is somewhat surprising that dynamic growth cones can utilize a sig-
naling system that establishes and maintains polarity in nonmoving cell sheets
such as in epithelia. However, at the molecular and cellular level, cell polar-
ity signaling may be similarly dynamic in both motile and nonmotile cells.
Recent studies suggest that components of adherens junctions, even
E-cadherin, are actively turned over even in these nonmoving cells
(
Baum & Georgiou, 2011
). The robustness of cell polarity signaling
