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used; additionally, connexin genes were disrupted to assess downstream
developmental effects. Still, few conclusions can be drawn regarding the spe-
cific role for connexins during preimplantation development, given some-
times conflicting results (
Davies et al., 1996; Houghton, 2005; Houghton
et al., 2002
). For example, neither connexin knockouts nor pharmacological
inhibition of connexins significantly disrupted development; in contrast,
antibody-mediated disruption of connexin perturbed compaction and blas-
tocyst development
(
Kidder
and Winterhager, 2001; Vance
and
Wiley, 1999
).
Human preimplantation embryos predominantly express connexin 43;
however, connexin expression patterns were found to vary among differ-
ent (human) embryos of normal morphology (
Bloor et al., 2004; Hardy
et al., 1996
). Furthermore, evidence suggests that gap junctions could
potentially control tight junction assembly and cell lineage divergence
(
Houghton, 2005; Toyofuku et al., 1998
). Protein kinase C signaling
could be involved in these processes, but different lines of evidence
demonstrate that there is still clarification needed in specifying its role
(
Eckert and Fleming, 2008
).
3.6. Cell junctions and the cytoskeleton in development
Embryonic morphogenesis requires a constant and precisely executed rem-
odeling of cell junctions. This process is accompanied by dramatic cytoskel-
etal remodeling that facilitates the changes in cell shape and motility (
Jamora
and Fuchs, 2002
). In preimplantation mammalian embryos, actin
cytoskeleton-associated adherens junctions and tight junctions appear at
the eight-cell stage, while the intermediate filament-associated desmosomal
emergence occurs at the 32-cell stage (
Eckert and Fleming, 2008
). A rich
body of evidence points to a precisely controlled cross-junctional force bal-
ance between intercellular adhesion and cortical tension in governing the
dynamics of cell junctions (
Lecuit and Lenne, 2007; Paluch and
Heisenberg, 2009
). Some important features of junctional mechanics during
morphogenesis have been characterized (
Hayashi and Carthew, 2004; Kafer
et al., 2007; Rauzi et al., 2008
). To some extent, embryonic morphogenesis
results largely from epithelial sheet stretching, contraction, migration, and
deformation (
Stepniak et al., 2009
). The mechanical forces generated by
dynamic rearrangements of cell junctions and the cytoskeleton thereby facil-
itate the morphological changes that transform flat cell sheets into three-
dimensional structures (
Jamora and Fuchs, 2002
).
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