Murine Wnt-11 and Wnt-12 have temporally and spatially restricted expression patterns during embryonic development

Christiansen, Jeffrey H.; Dennis, Carina L.; Wicking, Carol; Monkley, Susan J.; Wilkinson, David G.; Wainwright, Brandon

doi:10.1016/0925-4773(95)00383-5

Cited by 131 publications

(84 citation statements)

References 36 publications

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“…Some Wnt genes can behave in an oncogenic fashion, as exempli®ed by Wnt1 (Christiansen et al, 1996). While no Wnt gene mutations have been associated with Wilms' tumour and Wnt4 has never been reported to behave in this fashion, Koester and Ridder (1999) demonstrated that 15% (6 out of 40) of WTs, harbour heterozygous missense/microdeletion mutations in the b-catenin proto-oncogene.…”

Section: Discussionmentioning

confidence: 99%

Wnt-4 regulation by the Wilms' tumour suppressor gene, WT1

Sim

Smith

et al. 2002

Oncogene

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The Wilms' tumour suppressor gene, WT1, encodes multiple nuclear protein isoforms, all containing four C-terminal zinc ®nger motifs. WT1 proteins can both activate and repress putative target genes in vitro, although the in vivo relevance of these putative target genes is often unveri®ed. WT1 mutations can result in Wilms' tumour and the Denys-Drash Syndrome (DDS) of infantile nephropathy, XY pseudohermaphroditism and predisposition to Wilms' tumour. We have established stable transfectants of the mouse mesonephric cell line, M15, which express WT1 harbouring a common DDS point mutation (R394W). A comparison of the expression pro®les of M15 and transfectant C2A was performed using Nylon-based arrays. Very few genes showed di erential expression. However Wnt-4, a member of the Wnt gene family of secreted glycoproteins, was downregulated in C2A and other similar clones. Doxycycline induction of WT1-A or WT1-D expression in HEK293 stable transfectants also elicited an elevation in Wnt4 expression. Wnt4 is critical for the mesenchyme-to-epithelial transition during kidney development, making it an attractive putative WT1 target. We have mapped human Wnt-4 gene to chromosome 1p35-36, a region of frequent LOH in WT, have characterized the genomic structure of the human Wnt-4 gene and isolated 9 kb of immediate promoter. While several potential WT1 binding sites exist within this promoter, reporter analysis does not strongly support the direct regulation of Wnt4 by WT1. We propose that Wnt-4 regulation by WT1 occurs at a more distant promoter or enhancer site, or is indirect.

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Section: Discussionmentioning

confidence: 99%

Wnt-4 regulation by the Wilms' tumour suppressor gene, WT1

Sim

Smith

et al. 2002

Oncogene

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“…In cells responding to canonical Wnt signaling, ␤-catenin is stabilized and enters the nucleus to activate the Tcf/Lef family transcription factors and regulate transcription of downstream genes. Although several Wnt genes as well as Tcf1 and Lef1 are known to be expressed in the developing facial primordia (Gavin et al, 1990;Oosterwegel et al, 1993;Parr et al, 1993;Christiansen et al, 1995;Wang and Shackleford, 1996), a direct role for Wnt signaling in facial morphogenesis was not known until recently. In search for genes conferring susceptibility to spontaneous CLP in the A strains of mice, Juriloff and colleagues genetically mapped an essential causal recessive mutation, clf1, to a small region of mouse chromosome 11 containing the closely linked Wnt3 and Wnt9b genes (Juriloff and Mah, 1995;Juriloff et al, 1996Juriloff et al, , 2001.…”

Section: The Wnt Pathwaymentioning

confidence: 99%

Development of the upper lip: Morphogenetic and molecular mechanisms

Jiang

Bush

Lidral

2005

Developmental Dynamics

288

304

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The vertebrate upper lip forms from initially freely projecting maxillary, medial nasal, and lateral nasal prominences at the rostral and lateral boundaries of the primitive oral cavity. These facial prominences arise during early embryogenesis from ventrally migrating neural crest cells in combination with the head ectoderm and mesoderm and undergo directed growth and expansion around the nasal pits to actively fuse with each other. Initial fusion is between lateral and medial nasal processes and is followed by fusion between maxillary and medial nasal processes. Fusion between these prominences involves active epithelial filopodial and adhering interactions as well as programmed cell death. Slight defects in growth and patterning of the facial mesenchyme or epithelial fusion result in cleft lip with or without cleft palate, the most common and disfiguring craniofacial birth defect. Recent studies of craniofacial development in animal models have identified components of several major signaling pathways, including Bmp, Fgf, Shh, and Wnt signaling, that are critical for proper midfacial morphogenesis and/or lip fusion. There is also accumulating evidence that these signaling pathways cross-regulate genetically as well as crosstalk intracellularly to control cell proliferation and tissue patterning. This review will summarize the current understanding of the basic morphogenetic processes and molecular mechanisms underlying upper lip development and discuss the complex interactions of the various signaling pathways and challenges for understanding cleft lip pathogenesis.

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“…This once more raises the question of whether the placodes originate from a common structure, i.e., a mammary line. Guided by the knowledge that Lef1 (Van Genderen et al, 1994;Mailleux et al, 2002) and Wnt10b (Christiansen et al, 1995) are expressed in the mammary rudiments at E11.5-E12.5 and that the mammary rudiments are absent in E13.5 mouse embryos either lacking Lef1 expression (Van Genderen et al, 1994) or overexpressing the WNT inhibitor Dkk1 in the skin (Andl et al, 2002), we decided to examine the expression of Wnt genes in the mammary region of the mouse embryo by in situ hybridization. We show here that expression of Wnt10b precedes the appearance of mammary placodes.…”

Section: Introductionmentioning

confidence: 99%