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Bulk RNA-seq evaluation of in vitro cultured Sox9+ mouse lung progenitors isolated from E12.5 embryonic lung progenitors

ABSTRACT: Bulk RNA-seq evaluation of in vitro cultured Sox9+ mouse lung progenitors isolated from E12.5 embryonic lung progenitors

PROVIDER: PRJEB23065 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2174640.fastq.gz	Fastqsanger.gz
	ERR2174650.fastq.gz	Fastqsanger.gz
	ERR2174660.fastq.gz	Fastqsanger.gz
	ERR2174670.fastq.gz	Fastqsanger.gz
	ERR2174680.fastq.gz	Fastqsanger.gz

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Microarray evaluation of in vitro cultured Sox9+ mouse lung progenitors isolated from E12.5 embryonic lung progenitors

Project description:The study aims to show that Sox9+ Chd1+ mouse embryonic lung progenitors can be isolated and expanded long-term in 3D culture while maintaining their multipotency. in vitro cultured Sox9+ Chd1+ lung progenitors transcriptionally resemble their in vivo counterparts and show significant difference from adult lung epithelial (Cdh1+ and EpCAM+) and non-epithelial (Cdh1- and EpCAM-) cells

2017-11-01 | E-MTAB-6086 | biostudies-arrayexpress

Bulk RNA-seq evaluation of in vitro cultured Sox9+ mouse lung progenitors isolated from E12.5 embryonic lung progenitors

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Project description:This submission consists of two experiments utilizing translating ribosome affinity purification-sequencing (TRAP-seq). The first uses TRAP-seq to isolate transcripts from Sox9 positive progenitors at E14 and an E17 lung and compares it to non-immunoprecipitated whole lung homogenate control. The second compares TRAP-seq isolated transcripts from Sox9-wild type progenitors versus mutant progenitors. Recombination was induced at E13 and cells were isolated at E16.

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SOX9 modulates the expression of key transcription factors required for heart valve development

Project description:Heart valve formation initiates when endothelial cells of the heart transform into mesenchyme and populate the cardiac cushions. The transcription factor, SOX9, is highly expressed in the cardiac cushion mesenchyme, and is essential for heart valve development. Loss of Sox9 in mouse cardiac cushion mesenchyme alters cell proliferation, embryonic survival, and disrupts valve formation. Despite this important role, little is known regarding how SOX9 regulates heart valve formation or its transcriptional targets. Therefore, we mapped putative SOX9 binding sites by ChIP-Seq in embryonic day (E) 12.5 heart valves, a stage at which the valve mesenchyme is actively proliferating and initiating differentiation. Embryonic heart valves have been shown to express a high number of genes that are associated with chondrogenesis, including several extracellular matrix proteins and transcription factors that regulate chondrogenesis. Consequently, we compared regions of putative SOX9 DNA-binding between E12.5 heart valves and E12.5 limb buds. We identified context-dependent and contextâindependent SOX9 interacting regions throughout the genome. Analysis of context-independent SOX9 binding suggests an extensive role for SOX9 across tissues in regulating proliferation-associated genes including key components of the AP-1 complex. Integrative analysis of tissue-specific SOX9 interacting regions and gene expression profiles on Sox9-deficient heart valves demonstrated that SOX9 controls the expression of several transcription factors with previously identified roles in heart valve development, including Twist1, Sox4, Mecom/Evi1 and Pitx2. Together, our data identifies SOX9 coordinated transcriptional hierarchies that control cell proliferation and differentiation during valve formation. Examination of SOX9 binding sites in E12.5 atrioventricular canal (AVC) and E12.5 embryonic limb and mRNA expression profiling in E12.5 WT and Sox9 mutant AVCs, in duplicate.

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