Vertebrate Development Maternal to Zygotic Control (Advances in Experimental Medicine and Biology)

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et al. 1998 ; Boutros and Mlodzik 1999 ; Rothbächer et al. 2000 ). The N-terminal
DIX domain (Dishevelled, Axin) is critical for beta-catenin regulation whereas the
C-terminal DEP (Dvl, Egl-10, Pleckstrin) domain regulates PCP and calcium sig-
naling. In Drosophila, Dvl associates with Fzd1 and localizes to the distal cell mar-
gin. This complex inhibits the distal accumulation of Vang/Pk complexes, which are
restricted proximally.
In vertebrates, similar complexes are implicated but the assembly and asymme-
try of these is less understood. Fzd/Dvl association likely occurs following GPCR
activation, and Dvl and Fzds accumulate in asymmetric puncta in cells in various
vertebrate tissues undergoing PCP. In the zebrafish gastrula, Dvl-GFP is localized to
the posterior membrane of cells whereas injected Drosophila Prickle-GFP localizes
to the opposite, anterior edge (Ciruna et al. 2006 ; Yin et al. 2008 ). Additionally, in
the mouse posterior notochord/node, Prickle2 and Vangl1 colocalize at the anterior
edge of cells (Antic et al. 2010 ) and Dvl-GFP localizes posteriorly (Hashimoto et al.
2010 ). However, in other tissues such as the cochlea, Vangl2 and Fzd3 colocalize
(Wang and Nathans 2007 ), but Prickle2 and Fzd6 localize to opposite sides (Deans
et al. 2007 ). Celsr1 (a vertebrate Fmi homolog; cadherin, EGF LAG seven-pass
G-type receptor 1) may also play a role in recruiting Dvl/Fz complexes to adherens
junctions in the neural plate and mediating subsequent signaling (Nishimura et al.
2012 ). Thus in vertebrates, the roles of the different core PCP components may have
diverged following gene duplication and the acquisition of Wnt ligand dependence
and may have taken on tissue- or cell type-specific roles.
Dvl recruitment in the context of Wnt/PCP signaling is implicated in the control
of cytoskeletal dynamics through the activation of small GTPases. Dvl can recruit
the Formin-related Daam1 protein to activate Rho in an Wnt-dependent manner and
regulate actin dynamics (Habas et al. 2001 ). Additionally, Rho activation can lead to
Rho kinase (Rok2) activation to control cell shape (Marlow et al. 2002 ; Tahinci and
Symes 2003 ). In a separate and parallel pathway, Dvl can directly activate Rac
downstream of Wnt, leading the stimulation of filopodial extensions and Mapk8
(Jun N-terminal kinase, JNK) activation (Habas et al. 2003 ; Tahinci and Symes
2003 ). The coordinate activity of Rho and Rac, and potentially other small GTPases,
is required for cell intercalation and convergent extension morphogenesis in many
developing tissues.


6.3.1.4 Wnt/Calcium Release Signaling


Certain Wnt-Fzd combinations can stimulate the release of intracellular calcium
stores (reviewed in Veeman et al. 2003a; Kohn and Moon 2005 ) and signal indepen-
dently of beta-catenin. The regulation of this pathway also begins with Fzd-mediated
heterotrimeric G protein activation and involves well-characterized GPCR
responses, namely phosphoinositide turnover (Slusarski et al. 1997b), activation of
cGMP-phosphodiesterase (Ahumada et al. 2002 ), as well as Calmodulin-dependent
protein kinase 2 (Camk2) and Protein kinase C (Prkca) activation (Sheldahl et al.
1999 ; Kuhl et al. 2000 ). Many of the same coreceptors involved in Wnt/PCP


D.W. Houston

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