Frizzled 2 and frizzled 7 function redundantly in convergent extension and closure of the ventricular septum and palate: evidence for a network of interacting genes

Abstract

SUMMARY

RAP1-mediated MEK/ERK pathway defects in Kabuki syndrome

“…Our study suggests that the pathophysiology of KS overlaps with that of the RASopathies. The subcellular defects observed in our study might contribute not only to the skeletal defects in KS, but also to other KS-associated phenotypes, such as heart and renal defects, both of which have been observed in CE mutants with defective cell intercalation (38,39) and especially in rap1 morphants (40). Our data also demonstrate that the genetic defects in KS can have opposite effects, either activating or silencing, on the MAPK pathway, depending on whether the RAP1 proteins operate through BRAF or RAF1.…”

Canonical and noncanonical Wnt signaling in neural stem/progenitor cells

“…Adding to this complexity, the Wnt response can differ depending on cell context and on the repertoire of Wnt receptors 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 expressed [25,26], further underlining the importance of determining the "Wnt status" of cells. ROR2, for example, has been shown to activate phosphatidylinositol-3 kinase (PI3K), which in turn activates JNK and its associated transcription factors c-Jun and ATF2 in Xenopus [27,28].…”

Divergent roles for Wnt/β-catenin signaling in epithelial maintenance and breakdown during semicircular canal formation

“…The Wnt signaling pathway has been implicated in the fusion of several other tissues, including the neural tube, palate and ventricular septum (Pinson et al, 2000;Lee et al, 2008;Song et al, 2009;Song et al, 2010;Yu et al, 2012). However, a unifying theory for how Wnt signaling functions to mediate tissue fusion has yet to be elucidated and might very well be context dependent.…”