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

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Lrp6

Axin Apc

Pygo/

Bcl9

Tcf7l1 Prmt2

Groucho

Gsk3/

CKI

nucleus:: no target txn

Ctnnb1-p

ubiquitylation/

proteasomal

degradation

Btrc

Lrp6-p

Ptk7 Dkk1

Tiki

Notum

Wnt1

Wnt5 Ror2/Ryk

Fzd

Dvl

Vangl/Pk

Daam1/

Rho

Rok2

Mapk8

Rac1

PDE PLC

Cn

Prkca

Camk2

FAK

Map3k7

Nlk

Nfatc Ctnnb1

Axin Apc

Pygo/

Bcl9

Tcf7l1

Prmt2

Groucho

IP 3 /Ca2+

Gsk3/

CKI

[cGMP]

?

cell shape change

cell motility

filopodia

Jund/txn

nucleus::target txn

cell adhesion changes

+ Wnt

• Wnt

Fig. 6.7 Generalized Wnt signaling networks. In the absence of activating Wnt ligands (top panel,
-Wnt), beta-catenin protein (Ctnnb1) is phosphorylated by destruction complex components and
tagged for proteasomal degradation. In the nucleus, Tcf7l1/Tcf3 represses Wnt target promoter
activity through recruitment of Groucho. Upon stimulation with Wnt ligand, a variety of pathways
are activated (see text for details). Predominantly positive-acting components with respect to beta-
catenin regulation are shown in green, negative components in red, beta-catenin-independent com-
ponents are light blue. Beta-catenin is shown in yellow. Circles indicate component nodes, lines
indicate edges, or interacting components. This arrangement is not meant to convey specific exact
binding relationships or stoichiometry. Wnt1 is shown as a beta-catenin-activating ligand, whereas
Wnt5 is shown as a Wnt/PCP and Wnt/Calcium-stimulating ligand. Plot was generated with
iGraph in R (Csardi and Nepusz 2014 ). txn transcription

D.W. Houston

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