Sox17‐2A‐iCre: A knock‐in mouse line expressing Cre recombinase in endoderm and vascular endothelial cells

Engert, Silvia; Liao, Wenbin; Burtscher, Ingo; Lickert, Heiko

doi:10.1002/dvg.20540

Cited by 60 publications

(103 citation statements)

References 27 publications

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“…The Sox17 2AiCre allele, the β-catenin (Ctnnb1) floxed (F) and floxed deleted (FD) alleles were previously described (Brault et al, 2001;Engert et al, 2009; (Soriano, 1999). Mutant mice were bred on a mixed CD1×C57Bl/6 background.…”

Section: Generation Of Mutant Mice and Genotypingmentioning

confidence: 99%

“…Mutant mice were bred on a mixed CD1×C57Bl/6 background. PCR genotyping was performed on tail tip genomic DNA and embryonic tissue following lysis in buffer containing proteinase K as described (Engert et al, 2009). …”

Section: Generation Of Mutant Mice and Genotypingmentioning

confidence: 99%

“…To delete β-catenin in the Sox17 lineage, we used a crossing scheme in which males heterozygous for a β-catenin (Ctnnb1) floxed deleted (FD) allele (Brault et al, 2001; and the Sox17 2AiCre allele (Engert et al, 2009) were mated to females homozygous for the β-catenin floxed (F) allele and the R26 reporter (R26R) allele (Fig. 1E,F) (Soriano, 1999).…”

Section: Research Articlementioning

confidence: 99%

“…They further demonstrate that Sox17 + cells are already restricted to the endoderm lineage, as no cell fate switch to cardiac mesoderm occurred . However, the failure of Foxa2 induction in epiblast progenitors of the Sox17 lineage was unexpected (Engert et al, 2009) and suggests that both cell-autonomous and non-autonomous mechanisms contribute to the CKO mutant phenotype.…”

Section: Lack Of β-Catenin Affects Ve Patterning and De Formationmentioning

confidence: 99%

“…The cells fated to become DE emerge from a Foxa2 + epiblast population , ingress into the PS region and start to express Sox17 while they intercalate into and disperse the overlying VE (Burtscher et al, 2012;Kwon et al, 2008). After gastrulation, the Sox17 protein is restricted to the DE, the mid-and hindgut endoderm and the endothelial cells of the forming vasculature (Burtscher et al, 2012;Engert et al, 2009;Kanai-Azuma et al, 2002). Deletion of the Sox17 gene results in turning defects and posterior truncations at E8.5-9.5 due to defective mid-and hindgut development (Kanai-Azuma et al, 2002;Viotti et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Wnt/β-catenin signalling regulates Sox17 expression and is essential for organizer and endoderm formation in the mouse

et al. 2013

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Several signalling cascades are implicated in the formation and patterning of the three principal germ layers, but their precise temporal-spatial mode of action in progenitor populations remains undefined. We have used conditional gene deletion of mouse β-catenin in Sox17-positive embryonic and extra-embryonic endoderm as well as vascular endothelial progenitors to address the function of canonical Wnt signalling in cell lineage formation and patterning. Conditional mutants fail to form anterior brain structures and exhibit posterior body axis truncations, whereas initial blood vessel formation appears normal. Tetraploid rescue experiments reveal that lack of β-catenin in the anterior visceral endoderm results in defects in head organizer formation. Sox17 lineage tracing in the definitive endoderm (DE) shows a cell-autonomous requirement for β-catenin in midgut and hindgut formation. Surprisingly, wild-type posterior visceral endoderm (PVE) in midgut- and hindgut-deficient tetraploid chimera rescues the posterior body axis truncation, indicating that the PVE is important for tail organizer formation. Upon loss of β-catenin in the visceral endoderm and DE lineages, but not in the vascular endothelial lineage, Sox17 expression is not maintained, suggesting downstream regulation by canonical Wnt signalling. Strikingly, Tcf4/β-catenin transactivation complexes accumulated on Sox17 cis-regulatory elements specifically upon endoderm induction in an embryonic stem cell differentiation system. Together, these results indicate that the Wnt/β-catenin signalling pathway regulates Sox17 expression for visceral endoderm pattering and DE formation and provide the first functional evidence that the PVE is necessary for gastrula organizer gene induction and posterior axis development.

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Section: Generation Of Mutant Mice and Genotypingmentioning

confidence: 99%

Section: Generation Of Mutant Mice and Genotypingmentioning

confidence: 99%

Section: Research Articlementioning

confidence: 99%

Section: Lack Of β-Catenin Affects Ve Patterning and De Formationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Wnt/β-catenin signalling regulates Sox17 expression and is essential for organizer and endoderm formation in the mouse

et al. 2013

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Detailed phenotyping of Tbr1‐2A‐CreER knock‐in mice demonstrates significant impacts on TBR1 protein levels and axon development

Co,

O'Brien,

Wright

et al. 2024

Autism Research

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Cre recombinase knock‐in mouse lines have served as invaluable genetic tools for understanding key developmental processes altered in autism. However, insertion of exogenous DNA into the genome can have unintended effects on local gene regulation or protein function that must be carefully considered. Here, we analyze a recently generated Tbr1‐2A‐CreER knock‐in mouse line, where a 2A‐CreER cassette was inserted in‐frame before the stop codon of the transcription factor gene Tbr1. Heterozygous TBR1 mutations in humans and mice are known to cause autism or autism‐like behavioral phenotypes accompanied by structural brain malformations, most frequently a reduction of the anterior commissure (AC). Thus, it is critical for modified versions of Tbr1 to exhibit true wild‐type‐like activity. We evaluated the Tbr1‐2A‐CreER allele for its potential impact on Tbr1 function and complementation to Tbr1 loss‐of‐function alleles. In mice with one copy of the Tbr1‐2A‐CreER allele, we identified reduction of TBR1 protein in early postnatal cortex along with thinning of the AC, suggesting hypersensitivity of this structure to TBR1 dosage. Comparing Tbr1‐2A‐CreER and Tbr1‐null mice to Tbr1‐null complementation crosses showed reductions of TBR1 dosage ranging from 20% to 100%. Using six combinatorial genotypes, we found that moderate to severe TBR1 reductions (≥44%) were associated with cortical layer 5 expansion, while only the complete absence of TBR1 was associated with reeler‐like “inverted” cortical layering. In total, these results strongly support the conclusion that Tbr1‐2A‐CreER is a hypomorphic allele. We advise caution when interpreting experiments using this allele, considering the sensitivity of various corticogenic processes to TBR1 dosage and the association of heterozygous TBR1 mutations with complex neurodevelopmental disorders.

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Lineage tracing of the endoderm during oral development

Rothová

Thompson

Lickert

et al. 2012

Developmental Dynamics

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Background: The contribution of the endoderm to the oral tissues of the head has been debated for many years. With the arrival of Cre/LoxP technology endoderm progenitor cells can now be genetically labeled and tissues derived from the endoderm traced. Using Sox17-2A-iCre/Rosa26 reporter mice we have followed the fate of the endoderm in the teeth, glands, and taste papillae of the oral cavity. Results: No contribution of the endoderm was observed at any stage of tooth development, or in development of the major salivary glands, in the reporter mouse during development. In contrast, the minor mucous glands of the tongue were found to be of endodermal origin, along with the circumvallate papilla and foliate papillae. The mucous minor salivary glands of the palate, however, were of mixed ectodermal and endodermal origin. Conclusions: In contrast to urodele studies, the epithelium of murine teeth is derived solely from the ectoderm. The border between the ectoderm-and endoderm-derived epithelium may play a role in determining the position of the lingual glands and taste buds, and may explain differences observed between taste buds in the anterior and posterior part of the tongue. Developmental Dynamics 241:1183-1191, 2012. V C 2012 Wiley Periodicals, Inc.Key words: endoderm; oral cavity; lineage labeling; mouse; tooth; gland; taste buds Key findings:The epithelium of murine teeth is derived from the ectoderm. The epithelium of the major salivary glands is derived from the ectoderm. A V-shaped border at the base of the tongue separates the ectoderm-and endoderm-derived tissue. The minor mucous salivary glands of the tongue, circumvallate papillae, and foliate papillae are derived from endoderm.

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Sox17‐2A‐iCre: A knock‐in mouse line expressing Cre recombinase in endoderm and vascular endothelial cells

Cited by 60 publications

References 27 publications

Wnt/β-catenin signalling regulates Sox17 expression and is essential for organizer and endoderm formation in the mouse

Wnt/β-catenin signalling regulates Sox17 expression and is essential for organizer and endoderm formation in the mouse

Detailed phenotyping of Tbr1‐2A‐CreER knock‐in mice demonstrates significant impacts on TBR1 protein levels and axon development

Lineage tracing of the endoderm during oral development

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