Epithelial organs including the lung are known to possess regenerative abilities through activation of endogenous stem cell populations but the molecular pathways regulating stem cell expansion and regeneration are not well understood. Here we show that Gata6 regulates the temporal appearance and number of bronchioalveolar stem cells (BASCs) in the lung leading to the precocious appearance of BASCs and concurrent loss in epithelial differentiation in Gata6 null lung epithelium. This expansion of BASCs is the result of a dramatic increase in canonical Wnt signaling in lung epithelium upon loss of Gata6. Expression of the non-canonical Wnt receptor Fzd2 is down-regulated in Gata6 mutants and increased Fzd2 or decreased -catenin expression rescues, in part, the lung epithelial defects in Gata6 mutants. During lung epithelial regeneration, we show that canonical Wnt signaling is activated in the niche containing BASCs and forced activation of Wnt signaling leads to a dramatic increase in BASC numbers. Moreover, Gata6 is required for proper lung epithelial regeneration and postnatal loss of Gata6 leads to increased BASC expansion and decreased differentiation. Together, these data demonstrate that Gata6 regulated Wnt signaling controls the balance between stem/progenitor expansion and epithelial differentiation required for both lung development and regeneration.
A Gata6-Wnt pathway required for epithelial stem cell development and airway regeneration.
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View SamplesNeutrophils were isolated form peripheral blood of wildtype and Phd3 null mice, cultured for 4 hours in hypoxia (3% O2) and micro array analysis performed
Prolyl hydroxylase 3 (PHD3) is essential for hypoxic regulation of neutrophilic inflammation in humans and mice.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Prediction of miRNA-mRNA associations in Alzheimer's disease mice using network topology.
Sex, Age, Specimen part
View SamplesWe addressed the integrated analysis of mRNA and miRNA expression levels of Tg6799 AD model mice at 4 month and 8 months of age. Total 8 gene cluster modules for co-expression network were predicted from transcriptome data and 6 modules were show relation with AD or aging. We constructed early stage AD network using data integration between mRNA and miRNA profiles and predicted miRNAs strongly involved in module regulation. We found that ARRDC3 showed AD mutation dependent changes of expression and was related metabolic dysfunction in early stage AD.
Prediction of miRNA-mRNA associations in Alzheimer's disease mice using network topology.
Sex, Age, Specimen part
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View SamplesWe report quantitative transcriptome data in WT and CHD1 mutant. Overall design: RNA-seq in wild-type and CHD1 mutant.
The ATP-dependent chromatin remodeler Chd1 is recruited by transcription elongation factors and maintains H3K4me3/H3K36me3 domains at actively transcribed and spliced genes.
Genetic information, Subject
View Samples