Loss of Wnt8b has no overt effect on hippocampus development but leads to altered Wnt gene expression levels in dorsomedial telencephalon

Abstract

Wnt signalling proteins regulate many aspects of animal development. We have investigated the function of mouse Wnt8b during forebrain development. Wnt8b is expressed in a highly restricted pattern including the prospective hippocampus and hypothalamus. Mutant mice lacking Wnt8b are viable and healthy. The size and morphology of the hippocampus appeared normal in mutant embryos and adults, and we found no evidence of hypothalamic defects in mutants. Wnt8b is also expressed in the neurogenic region of the adult dentate gyrus, however, cell proliferation was unchanged in Wnt8b 2/2 mutants. Mutant embryos did, however, display altered levels of expression of other Wnt genes normally expressed in forebrain. The spatial expression patterns of other Wnt genes and the overall level of canonical Wnt activity were indistinguishable from wild-types. Thus, loss of Wnt8b does not give rise to an overt morphological phenotype, but does affect expression levels of other Wnts in developing forebrain. Developmental Dynamics 239:284-296,

WT1 controls antagonistic FGF and BMP-pSMAD pathways in early renal progenitors

“…Indeed, we observed a marked reduction of Wnt8b (7.4 Â ; P ¼ 5.0e À 7; Student's t-test) and Rspo1 (6.3 Â ; P ¼ 9.5e À 9; Student's t-test) expression. According to Gudmap and Eurexpress databases, Wnt8b expression is relatively low in developing kidneys, and since Wnt8b mutants are phenotypically normal 41 , we did not further investigate its potential role in kidney development. Rspondins encode important regulators of canonical b-catenin signalling by binding to leucine-rich repeatcontaining G protein-coupled receptors 42 .…”

A Comprehensive Overview of Skeletal Phenotypes Associated with Alterations in Wnt/β-catenin Signaling in Humans and Mice

“…Because Wnts were initially characterized for their importance in body patterning in Drosophila and Xenopus (167,168), it is not surprising that mutation of individual Wnt proteinsin mice results in either failure of axial body patterning (Wnt1, 3, 3a, 5a, and 8a) (66, 71, 76,163,165) and/or abnormal limb development (Wnt3, 5a, 7a, 9a) (64, 69, 71, 74). However, most Wnts appear to have at best a redundant rolein body patterning in the mouse; they may have more critical roles in the development of specific organs or tissues (Wnt2, 2b, 4, 5b, 6, 7b, 8b, 9b, 10b, 11, 83,166,(169)(170)(171)(172)(173)(174)(175)(176) Overexpression of a Wnt10b transgene with the Fabp4 adipocyte-specific promoter enhanced trabecular bone formation and the mechanical properties of long bones. This is likely a consequence of expression from the bone marrow compartment (81).…”

Ofd1 Controls Dorso-Ventral Patterning and Axoneme Elongation during Embryonic Brain Development

“…Similarly to Pax6 and Ngn2 , Lhx2 expression has lost its expression gradient, but is still maintained in the malformed cortex, and not ectopically expressed in the protruded dorsomedial structure in severely affected Ofd1 Δ 4–5/+ mutant embryos (red arrows in Figure 2F). Finally, we assessed the expression of Wnt8b , which is expressed in dorsomedial cortical structures, but not in the cortical primordium (Figure 2G) [33], [34]. Severely affected O fd1 Δ 4–5/+ mutant embryos showed only a slight expansion of Wnt8b expression dorsomedially (red arrows in Figure 2H), indicating that the abnormally protruded dorsomedial structure in mutant embryos has not a cortical origin.…”