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Single cell RNA sequencing of embryonic thymuses from 22q11.2 DS mouse models following in utero drug treatments.

ABSTRACT: 22q11.2 DS causes the formation of a hypoplastic thymus. Mouse models of 22q11.2 were used to study the impact of different drugs, administered in pregnant mice, on the growth of the thymus. Thymuses from the different treatments were processed for single cell RNA sequencing. These were from control (Tbx1+/+;+/neo2) and 22q mouse models (Tbx1neo2/neo2 )

ORGANISM(S): Mus musculus

PROVIDER: GSE272825 | GEO | 2025/07/28

REPOSITORIES: GEO

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Single cell sequencing of e13 Embryonic Thymuses

Project description:Purpose: To identify and compare all the cell subsets present in Normal and 22q11.2 DS Hypoplastic thymus We have identified 17 distinct cell clusters in normal e13 embronic thymus. While both normal and 22q11.2 DS Hypoplastic thymus have same number of cell clusters, the trancriptome pattern varies significantly between them. Our scRNA sequencing results provide mesenchymal cells driven thymus hypoplasticity in 22q11.2 DS thymus.

2021-03-28 | GSE170686 | GEO

Single cell RNA sequencing of embryonic thymuses from 22q11.2 DS mouse models following in utero drug treatments.

Project description:Single cell RNA sequencing of embryonic thymuses from 22q11.2 DS mouse models following in utero drug treatments.

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Reduced dosage of Î²-catenin genetically rescues intracardiac anomalies in a Tbx1 conditional null mouse model of 22q11.2 deletion syndrome

Project description:Approximately 60-70% of patients with 22q11.2 deletion syndrome (22q11.2DS; velo-cardio-facial syndrome/DiGeorge syndrome) have cardiac outflow tract anomalies including persistent truncus arteriosus (PTA) as the most severe defect. Among the genes in the 22q11.2 region, TBX1, encoding a T-box transcription factor is a major candidate for cardiovascular malformations and its inactivation in mice results in a PTA. To identify novel signaling mechanisms that function downstream, we found that Tbx1 restricts canonical Wnt signaling in the pharyngeal apparatus. To test for tissue specificity within the pharyngeal apparatus, we inactivated Tbx1 in the anterior portion of the secondary heart field (AHF) mesoderm using the Mef2c-AHF-Cre allele and observed a full penetrant PTA (n = 30). Tbx1 promotes progenitor cells but restricts differentiation whereas Wnt signaling, in the AHF, promotes cardiomyocyte differentiation. To determine whether Tbx1 and canonical Wnt signaling act in opposing pathways, both alleles of Tbx1 and one Î²-catenin allele were inactivated in the AHF and 85% of them (n = 35) showed partial or complete rescue. The antagonistic function of the two pathways was further confirmed by gene expression profiling, indicating that these two pathways provide a key balance in the AHF to prevent premature differentiation of progenitor cells prior to reaching the cardiac outflow tract. We inactivatedTbx1 and beta-catenin allele to identify function of Tbx1 and beta-catenin in the anterior portion of the secondary heart field (AHF) mesoderm. We also inactivated both alleles of Tbx1 and one Î²-catenin alleles (rescue design) to determine whether Tbx1 and canonical Wnt signaling act in opposing pathways

2016-09-01 | E-GEOD-78125 | biostudies-arrayexpress

Reduced dosage of β-catenin genetically rescues intracardiac anomalies in a Tbx1 conditional null mouse model of 22q11.2 deletion syndrome

Project description:Approximately 60-70% of patients with 22q11.2 deletion syndrome (22q11.2DS; velo-cardio-facial syndrome/DiGeorge syndrome) have cardiac outflow tract anomalies including persistent truncus arteriosus (PTA) as the most severe defect. Among the genes in the 22q11.2 region, TBX1, encoding a T-box transcription factor is a major candidate for cardiovascular malformations and its inactivation in mice results in a PTA. To identify novel signaling mechanisms that function downstream, we found that Tbx1 restricts canonical Wnt signaling in the pharyngeal apparatus. To test for tissue specificity within the pharyngeal apparatus, we inactivated Tbx1 in the anterior portion of the secondary heart field (AHF) mesoderm using the Mef2c-AHF-Cre allele and observed a full penetrant PTA (n = 30). Tbx1 promotes progenitor cells but restricts differentiation whereas Wnt signaling, in the AHF, promotes cardiomyocyte differentiation. To determine whether Tbx1 and canonical Wnt signaling act in opposing pathways, both alleles of Tbx1 and one β-catenin allele were inactivated in the AHF and 85% of them (n = 35) showed partial or complete rescue. The antagonistic function of the two pathways was further confirmed by gene expression profiling, indicating that these two pathways provide a key balance in the AHF to prevent premature differentiation of progenitor cells prior to reaching the cardiac outflow tract.

2016-09-01 | GSE78125 | GEO

Tbx1 haploinsufficiency induces bone-to-cerebellar deformity in 22q11.2 deletion syndrome

Project description:22q11.2 deletion syndrome (22q11DS) substantially increases the risk of cognitive decline and psychiatric disease. However, neuroanatomic changes in 22q11DS are of a subtle-to-moderate degree and their connection to brain function is not clear. Here we report a severe (~70%) and specific reduction (dysplasia) of two cerebellar lobules, paraflocculus and flocculus (PF/F) and associated deficits in vestibulo-ocular reflex (VOR) in mouse models of 22q11DS (22q11DS mice). A specific but less severe PF/F dysplasia was confirmed in humans with 22q11DS. Tbx1 haploinsufficiency recapitulated the PF/F and VOR deficits in 22q11DS mice. The 22q11DS-associated PF/F dysplasia was not due to altered neural composition or neurogenesis. Rather, a part of temporal bone called subarcuate fossa (SF), which encapsulates the PF/F, and semicircular canals of the inner ear, which connects to the SF were malformed in 22q11DS and Tbx1-deficientmice. Our single-nuclei RNA Sequencing and immunohistochemistry data revealed that Tbx1 haploinsufficiency caused precocious differentiation of chondrocyte to osteoblasts in the petrous bone, but no changes in cell type compositions in the PF/F. These data suggest a novel structure-function pathogenic interrelationship in 22q11DS, where Tbx1 haploinsufficiency causes a skeletal deformity occluding cerebellar development and resulting in motor learning deficiency.

2024-09-19 | GSE254044 | GEO

Gene profiling on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos E9.5

2014-05-21 | GSE35013 | GEO

Gene profiling on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos

2014-05-21 | GSE30980 | GEO

Gene profiling on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos E9.5

Project description:Velo-cardio-facial syndrome/DiGeorge syndrome/22q11.2 deletion syndrome (22q11DS) patients have a submucous cleft palate, velo-pharyngeal insufficiency associated with hypernasal speech, facial muscle hypotonia and feeding difficulties. Inactivation of both alleles of mouse Tbx1, encoding a T-box transcription factor, deleted on 22q11.2, results in a cleft palate and a reduction or loss of branchiomeric muscles. To identify genes downstream of Tbx1 for myogenesis, gene profiling was performed on mandibular arches (MdPA1) from Tbx1+/+ and Tbx1-/- mouse embryos. To obtain enough RNA for microarray hybridization experiments, dissected mandibular arches from three Tbx1+/+ and three Tbx1-/- E9.5 embryos were pooled according to genotype, with three microarrays performed in total per genotype. Affymetrix Mouse Gene ST 1.0 arrays (Affymetrix) were used. Hybridization, washing, staining and scanning were performed in the Genomics Core at Einstein (http://www.einstein.yu.edu/genetics/CoreFacilities.aspx?id=23934) according to the Affymetrix manual.

2014-05-21 | E-GEOD-35013 | biostudies-arrayexpress

Tbx1 haploinsufficiency induces bone-to-cerebellar deformity in 22q11.2 deletion syndrome

Project description:Tbx1 haploinsufficiency induces bone-to-cerebellar deformity in 22q11.2 deletion syndrome

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Identification of open chromatin regions in mouse cardiopharyngeal mesoderm

Project description:In the heart development, mesodermal progenitor cells in pharyngeal apparatus, termed cardiopharyngeal mesoderm, contribute to both atruim and right ventricle. Tbx1 gene, encoding a T-box transctiption factor and gene haploinsufficient in 22q11.2 deletion syndrome, is required for cardiac outflow tranct and branchiomeric muscle development. To understand how TBX1 affect open chromatin status in cardiopharyngeal mesoderm, we performed ATAC-seq in Tbx1-Cre lineage with/without Tbx1 expression.

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