E-GEOD-6662
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA98623
PROVIDER: E-GEOD-6662 | ExpressionAtlas | 2014-10-10
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-6662-analysis-methods.tsv | Tabular | |||
| E-GEOD-6662-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-6662-configuration.xml | Xml | |||
| E-GEOD-6662-percentile-ranks.tsv | Tabular | |||
| E-GEOD-6662.condensed-sdrf.tsv | Tabular |
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Project description:Rationale: 22q11 deletion syndrome arises from recombination between low copy repeats on chromosome 22. Typical deletions result in hemizygosity for TBX1 associated with congenital cardiovascular disease. Deletions distal to the typically deleted region result in a similar cardiac phenotype but lack extra-cardiac features of the syndrome suggesting that a second haploinsufficient gene maps to this interval. Objective: The transcription factor HIC2 is lost in most distal deletions as well as a minority of typical deletions. We used mouse models to test the hypothesis that HIC2 hemizygosity causes congenital heart disease. Methods and Results: We created a genetrap mouse allele of Hic2. The genetrap reporter was expressed in the heart throughout the key stages of cardiac morphogenesis. Homozygosity for the genetrap allele was embryonic lethal before embryonic day E10.5 while the heterozygous condition exhibited a partially penetrant late lethality. One third of heterozygous embryos had a cardiac phenotype. Magnetic resonance imaging demonstrated a ventricular septal defect with overriding aorta. Conditional targeting indicated a requirement for Hic2 within the Nkx2.5+ and Mesp1+ cardiovascular progenitor lineages but not in the Wnt1+ neural crest or Mef2c+ second heart field lineages. Microarray analysis revealed increased expression of BMP10. Conclusions: Our results demonstrate a novel role for Hic2 in cardiac development. Hic2 is the first gene within the distal 22q11 interval to have a demonstrated haploinsufficient cardiac phenotype in mice. Together our data suggests HIC2 haploinsufficiency likely contributes to the cardiac defects seen in distal 22q11 deletion syndrome. The aim of this microarray experiment was to compare gene expression changes in the E13.5 mouse heart in a conditional knockout of Hic2 (Mesp1Cre/+; Hic2FL/FL) against control. All samples represent pools of isolated hearts from E13.5 mouse embryos. 3 replicates of each genotype were assayed. The genotypes are: 'WT' (Hic2FL/FL) 'KO' (Mesp1Cre/+; Hic2 FL/FL)
2014-04-02 | E-GEOD-56430 | biostudies-arrayexpress
Project description:LRRC10 is a heart-specific gene required for proper cardiac function. The effects of Lrrc10 deletion on gene expression in the adult mouse heart was investigated. Lrrc10 knockout mice or wildtype controls, housed in 12 hour light:12 dark, ad lib feeding and drinking conditions were sacrificed at two months of age for cardiac gene expression analysis. A two color, reference design experiment in which heart RNA from 2 Lrrc10 knockout mice was pooled and labeled with Cy5 and hybridized according to Agilent protocols against a reference pool of RNA madeup from respective tissue taken from 2 month wildtype mice which was labeled with Cy3.
2012-03-15 | E-GEOD-36508 | biostudies-arrayexpress
Project description:LRRC10 is a heart-specific gene required for proper cardiac function. The effects of Lrrc10 deletion on gene expression in the embryonic mouse heart was investigated. Pregnant heterozygous Lrrc10 knockout mice (Lrrc10+/-) mated to male heterozygous knockouts (Lrrc10+/-), housed in 12 hour light:12 dark, ad lib feeding and drinking conditions, were sacrificed at embryonic day 15.5 (E15.5) and embryonic hearts were dissected for cardiac gene expression analysis. A two color, reference design experiment in which heart RNA from 2 Lrrc10 homozygous knockout embryos (Lrrc10-/-) were pooled and labeled with Cy5 and hybridized according to Agilent protocols against a reference pool of RNA madeup from respective tissue taken from littermate E15.5 wildtype (Lrrc10+/+) hearts and labeled with Cy3.
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Project description:Rationale: 22q11 deletion syndrome arises from recombination between low copy repeats on chromosome 22. Typical deletions result in hemizygosity for TBX1 associated with congenital cardiovascular disease. Deletions distal to the typically deleted region result in a similar cardiac phenotype but lack extra-cardiac features of the syndrome suggesting that a second haploinsufficient gene maps to this interval. Objective: The transcription factor HIC2 is lost in most distal deletions as well as a minority of typical deletions. We used mouse models to test the hypothesis that HIC2 hemizygosity causes congenital heart disease. Methods and Results: We created a genetrap mouse allele of Hic2. The genetrap reporter was expressed in the heart throughout the key stages of cardiac morphogenesis. Homozygosity for the genetrap allele was embryonic lethal before embryonic day E10.5 while the heterozygous condition exhibited a partially penetrant late lethality. One third of heterozygous embryos had a cardiac phenotype. Magnetic resonance imaging demonstrated a ventricular septal defect with overriding aorta. Conditional targeting indicated a requirement for Hic2 within the Nkx2.5+ and Mesp1+ cardiovascular progenitor lineages but not in the Wnt1+ neural crest or Mef2c+ second heart field lineages. Microarray analysis revealed increased expression of BMP10. Conclusions: Our results demonstrate a novel role for Hic2 in cardiac development. Hic2 is the first gene within the distal 22q11 interval to have a demonstrated haploinsufficient cardiac phenotype in mice. Together our data suggests HIC2 haploinsufficiency likely contributes to the cardiac defects seen in distal 22q11 deletion syndrome. the aim of this microarray experiment was to compare gene expression changes in the E13.5 mouse heart in a conditional knockout of Hic2 (Mesp1Cre/+; Hic2FL/FL) against control.
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