Tbx1 binding site in whole mouse embryo at E9.5 from in vivo ChIP-seq
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA725883 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14349214_1.fastq.gz | Fastqsanger.gz | |||
| SRR14349214_2.fastq.gz | Fastqsanger.gz | |||
| SRR14349215_1.fastq.gz | Fastqsanger.gz | |||
| SRR14349215_2.fastq.gz | Fastqsanger.gz | |||
| SRR14349216_1.fastq.gz | Fastqsanger.gz |
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Project description:We generated Avidin tag inserted at 3' end of Tbx1 using CRISPR/Cas9 genomic engineering and crossed them with BirA mice from the Jackson laboratory. After established double homozygous mouse colony, total twenty embryos at E9.5 were collected for each samples. After extraction of nucleus, Tbx1 binding regions were captured with Dynabeads™ MyOne™ Streptavidin T1.
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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.
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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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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.
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Project description:This study was aimed at identifying Tbx1 dosage-dependent genes in vivo, so we performed a transcriptome analysis of Tbx1 mutants with nine different genotypes corresponding to different Tbx1 mRNA dosages. RNA isolated from whole E9.5 embryos with 9 different genotypes was hibridized to Affymetrix GeneChip Mouse Genome 430 2.0 arrays. For each genotype, we used two embryos (biological replicates), each hybridized to one array, thus we analyzed a total of 18 arrays. Tbx1 gene dosage
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Project description:Transcriptional profiling of E9.5 mouse embryo tissue from the presomitic mesoderm (PSM) and somites I-IV. Tissue from embryos lacking a functional Paraxis gene (Paraxis-/-) was compared to identical tissue from E9.5 Wild Type embryos. The goal was to identify genes that had become deregulated in the absence of the transcription factor, Paraxis.
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Project description:Transcriptional profiling of E9.5 mouse embryo tissue from the presomitic mesoderm (PSM) and somites I-IV. Tissue from embryos lacking a functional Paraxis gene (Paraxis-/-) was compared to identical tissue from E9.5 Wild Type embryos. The goal was to identify genes that had become deregulated in the absence of the transcription factor, Paraxis. Two-condition experiment: WT vs Paraxis-/- tissue. Biological replicates: 3 pools of 5 WT samples, 3 pools of 5 Paraxis-/- samples. Technical replicates: 3 dye swaps.
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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.
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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-/- E10.5 embryos were pooled according to genotype, with three microarrays performed in total per genotype. The tissue was homogenized in Buffer RLT (QIAGEN). Total RNA was isolated with the RNeasy Micro Kit according to the manufacturer’s protocol. Quality and quantity of total RNA was determined using an Agilent 2100 Bioanalyzer (Agilent) and an ND-1000 Spectrophotometer (NanoDrop), respectively. Biotinylated single-stranded cDNA targets were amplified from 100 nanograms (ng) starting total RNA using the Ovation RNA Amplification System V2 and FL- Ovation cDNA Biotin Module V2 (NuGEN). A total of 3.75 ?g of cDNA from the last step was hybridized to the GeneChip Test3 array (Affymetrix) to test the quality of the labeled target. Nucleic acid samples that passed quality control were then hybridized to the GeneChip Mouse Genome 430 2.0 Arrays (Affymetrix). 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.
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