Dataset Information


Whole heart transcriptional response to complete and epiblast-specfic deletion of Zic3 in 15.5 dpc mouse embryos

ABSTRACT: In order to better understand the molecular basis for the heart defects seen in Zic3 null and epiblast CKO embryos, we investigated whether complete or epiblast-specific deletion of Zic3 would impact later embryonic heart development at the transcriptional level by whole genome expression microarray. The whole heart was carefully dissected out from 15.5 dpc Zic3 +/y, Zic3 flox/y, Zic3 flox/y; Sox2-cre, and Zic3 -/y embryos, total RNAs were extracted and purified using RNeasy Mini Kit (QIAGEN). Spectrophotometry (NanoDrop-1000 Spectrophotometer, Thermo Fisher Scientific) and microfluidic electrophoresis (Experion Automated Electrophoresis System, Bio-Rad Laboratories) were used for RNA quality control. In vitro transcription was performed using Illumina TotalPrep RNA Amplification Kit (Applied Biosystems/Ambion). cRNAs were hybridized onto Illumina MouseWG-6 v2.0 Expression BeadChips (Illumina) per manufacturer’s instructions.

ORGANISM(S): Mus musculus  

SUBMITTER: John W Belmont   Zhengxin Jiang 

PROVIDER: E-GEOD-41674 | ArrayExpress | 2012-12-12



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Zic3 is required in the extra-cardiac perinodal region of the lateral plate mesoderm for left-right patterning and heart development.

Jiang Zhengxin Z   Zhu Lirong L   Hu Lingyun L   Slesnick Timothy C TC   Pautler Robia G RG   Justice Monica J MJ   Belmont John W JW  

Human molecular genetics 20121125 5

Mutations in ZIC3 cause human X-linked heterotaxy and isolated cardiovascular malformations. A mouse model with targeted deletion of Zic3 demonstrates an early role for Zic3 in gastrulation, CNS, cardiac and left-right axial development. The observation of multiple malformations in Zic3(null) mice and the relatively broad expression pattern of Zic3 suggest its important roles in multiple developmental processes. Here, we report that Zic3 is primarily required in epiblast derivatives to affect le  ...[more]

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