The Wnt signaling mediator tcf1 is required for expression of foxd3 during Xenopus gastrulation

Janssens, Sylvie; Broek, Olaf van den; Davenport, Ian; Akkers, Robbert C.; Liu, Fei; Veenstra, Gert Jan C.; Hoppler, Stefan; Vleminckx, Kris; Destrée, Olivier

doi:10.1387/ijdb.120191kv

Cited by 9 publications

(5 citation statements)

References 41 publications

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“…The results presented here for XTcf1B and XTcf1D confirm and extend earlier results (Janssens et al, 2013). Activation of direct target genes after Tcf1 B or D overexpression, like Foxd3 (Janssens et al, 2013), is supposed to take place through Wntresponsive elements, after recruitment of b-catenin (Logan and Nusse, 2004;Cadigan and Waterman, 2012;Schuijers et al, 2014).…”

Section: Differences In Response To Ectopic Overexpression Of Xtcf1 Isupporting

confidence: 88%

Functional differences between Tcf1 isoforms in early Xenopus development

Roël

Broek²,

Destrée³

2017

Int. J. Dev. Biol.

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In Xenopus gastrula stage embryos, four isoforms of Tcf1 (B, C, D and E) are present with high amino acid sequence conservation compared to fish, mice and human. We studied possible functional differences between these Tcf1 isoforms during early Xenopus development. After overexpression of single Tcf1 isoforms, two distinct phenotypes were observed. Overexpression of the B or D isoforms of Tcf1, which both lack a C-clamp, enhances early canonical Wnt signaling and induces ectopic dorsal mesoderm at the expense of ventrolateral mesoderm prior to gastrulation, causing severe antero-dorzalization of embryos. Overexpression of the E-isoform, which contains a complete C-clamp, does not induce ectopic dorsal mesoderm, but rather leads to severe caudal truncation. Overexpression of the C-isoform, which contains a partial C-clamp, induces a similar phenotype. Mutation of a single amino acid in the C-clamp, known to produce a hypomorphic mutant in D. melanogaster, led to a gain of function in inducing ectopic organizer tissue, as observed after overexpression of the B or D isoforms of Tcf1. Depletion of the C-clamp exon from the zygotic mRNA pool, by injection of a morpholino oligo that targets the splice acceptor site of the exon containing the C-clamp, caused a severe shortening of the AP-axis. Furthermore, embryos showed poor development of the CNS, paraxial mesoderm and primary blood vessels. In situ hybridization analysis showed that Lef1 expression was downregulated at the mid-hindbrain boundary, in the otic vesicles and the branchial arches. The results indicate that in post-gastrula stage Xenopus embryos, the E-tail of Tcf1 is required for expression of Lef1 and for blood vessel formation.

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Section: Differences In Response To Ectopic Overexpression Of Xtcf1 Isupporting

confidence: 88%

Functional differences between Tcf1 isoforms in early Xenopus development

Roël

Broek²,

Destrée³

2017

Int. J. Dev. Biol.

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“…The TCF/LEF family regulates gene expression of WNT/β‐catenin signaling downstream targets (Cadigan, ). For example, the TCF1 protein regulates gene expression of foxd3 , a transcriptional repressor of the winged helix or “Forkhead” family of proteins, during Xenopus gastrulation (Janssens et al, ). Foxd3 is expressed in premigratory and migrating NC cells and is one of the earliest molecular markers of the NC lineage (Teng et al, ).…”

Section: Molecular Mechanisms Of Midfacial Developmental Defectsmentioning

confidence: 99%

Molecular mechanisms of midfacial developmental defects

Suzuki

Sangani

Ansari

et al. 2015

Developmental Dynamics

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The morphogenesis of midfacial processes requires the coordination of a variety of cellular functions of both mesenchymal and epithelial cells to develop complex structures. Any failure or delay in midfacial development as well as any abnormal fusion of the medial and lateral nasal and maxillary prominences will result in developmental defects in the midface with a varying degree of severity, including cleft, hypoplasia, and midline expansion. In spite of the advances in human genome sequencing technology, the causes of nearly 70 percent of all birth defects, which include midfacial development defects, remain unknown. Recent studies in animal models have highlighted the importance of specific signaling cascades and genetic-environmental interactions in the development of the midfacial region. This review will summarize the current understanding of the morphogenetic processes and molecular mechanisms underlying midfacial birth defects based on mouse models with midfacial developmental abnormalities.

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“…Accordingly, FOXA2 has been linked to the pathogenesis of prostate and liver cancer [ 138 , 139 ], which could be explained in part by dysregulated Wnt signaling. Others have demonstrated the regulation of FOXC1/2, FOXD3, FOXJ1, and FOXN1 expression by β-catenin/TCF in different contexts [ 140 , 141 , 142 , 143 ], but the relevance for cancer biology is less clear in these cases.…”

Section: Forkhead Box Family Transcription Factorsmentioning

confidence: 99%

Regulation of Wnt Signaling by FOX Transcription Factors in Cancer

Koch

2021

Cancers

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Aberrant activation of the oncogenic Wnt signaling pathway is a hallmark of numerous types of cancer. However, in many cases, it is unclear how a chronically high Wnt signaling tone is maintained in the absence of activating pathway mutations. Forkhead box (FOX) family transcription factors are key regulators of embryonic development and tissue homeostasis, and there is mounting evidence that they act in part by fine-tuning the Wnt signaling output in a tissue-specific and context-dependent manner. Here, I review the diverse ways in which FOX transcription factors interact with the Wnt pathway, and how the ectopic reactivation of FOX proteins may affect Wnt signaling activity in various types of cancer. Many FOX transcription factors are partially functionally redundant and exhibit a highly restricted expression pattern, especially in adults. Thus, precision targeting of individual FOX proteins may lead to safe treatment options for Wnt-dependent cancers.

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The Wnt signaling mediator tcf1 is required for expression of foxd3 during Xenopus gastrulation

Cited by 9 publications

References 41 publications

Functional differences between Tcf1 isoforms in early Xenopus development

Functional differences between Tcf1 isoforms in early Xenopus development

Molecular mechanisms of midfacial developmental defects

Regulation of Wnt Signaling by FOX Transcription Factors in Cancer

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