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A phenotypic rescue approach identifies lineage regionalization defects in a mouse model of DiGeorge syndrome.

ABSTRACT: Evaluate the effect of the vB12 treatment on transcriptional profile of Tbx1 haploinsufficiency embryos we performed RNA-seq on whole E9.5 mouse embryos (21 somite stage) after treatment with vB12 (cyanocobalamin Sigma-Aldrich Prod. Number V2876) or vehicle (PBS) during pregnancy

ORGANISM(S): Mus musculus

PROVIDER: GSE206737 | GEO | 2022/09/07

REPOSITORIES: GEO

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Cardiac Outflow tract septation defects in a DiGeorge syndrome model respond to Minoxidil treatment

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Transcription profiling of mouse embryonic cells (E9.5) with homozygous knockout of Tbx1 compared to heterozygous Tbx1 knockout

Project description:22q11 deletion syndrome (22q11DS) is mainly characterised by cardiovascular, craniofacial, thymic and parathyroid abnormalities. Haploinsufficiency of the transcription factor, TBX1 is considered to be a major underlying cause of these defects. Mice in which Tbx1 has been mutated phenocopy 22q11DS. In order to elucidate the transcriptional pathways regulated by Tbx1, the gene expression profile of Tbx1-lacZ positive cells isolated from E9.5 Df1/Tbx1lacZ embryos (Tbx1-null) were compared to cells isolated from Tbx1+/lacZ (Tbx1-heterozygous) embryos. This analysis has led to a better understanding of the pathways important in pharyngeal and heart development. Experiment design: 3 pools of cells (biological replicates) isolated from Df1/Tbx1lacZ embryos and Tbx1+/lacZ embryos were used for hybridisation onto 6 MOE430 v2 oligonucleotide array chips (Affymetrix), making 12 microarrays in total. Each pool of cells was isolated from at least 8 embryos.

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Mus musculus

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

| PRJNA151171 | ENA

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