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SRP050224
Arabidopsis thaliana
12 Downloadable Samples
Illumina HiSeq 2500
Description
The correlation coefficient (R) for the expression profile of all transcripts between WT and asr3-1, and between WT and OX9 without flg22 treatment is close to linear, suggesting that ASR3 does not affect general gene transcription. Hierarchical clustering analysis flg22-induced genes in any of the three genotypes suggested that the asr3-1 mutant displayed overall enhanced flg22 response whereas OX9 displayed overall reduced responses compared to WT plants. Overall design: RNA-seq analysis was performed with 10-day-old seedlings of WT, asr3-1 and 35S:ASR3-HA transgenic line OX9 with or without 100 nM flg22 treatment for 30 min. Two independent repeats were performed for RNA-seq analysis. For each repeat, equal amount of RNA from two biological replicates was pooled for RNA-seq library construction. RNA-seq library preparation and sequencing were carried out on an Illumina HiSeq 2500 platform with 100 nt single end reads.
Publication Title
Phosphorylation of trihelix transcriptional repressor ASR3 by MAP KINASE4 negatively regulates Arabidopsis immunity.
Sample Metadata Fields
Specimen part, Subject
View Samples- Sus scrofa
- 6 Downloadable Samples
Affymetrix Porcine Genome Array (porcine)
Description
Porcine reproductive and respiratory syndrome (PRRS), caused by PRRS virus (PRRSV), is the most economically important disease in pig populations. Lung damage is one major pathological condition following PRRSV infection, often leading to animal death. In vivo, PRRSV productive infection occurs predominately in alveolar macrophages of the lung.
Publication Title
Molecular characterization of transcriptome-wide interactions between highly pathogenic porcine reproductive and respiratory syndrome virus and porcine alveolar macrophages in vivo.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Homo sapiens
- 17 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
The maturation of dendritic cells (DCs) after exposure to microbial products or inflammatory mediators plays a critical role in initiating the immune response. We found that maturation can also occur under steady state conditions, triggered by alterations in E-cadherin-mediated DC-DC adhesion. Selective disruption of these interactions induced the typical features of DC maturation including the upregulation of costimulatory molecules, MHC class II, and chemokine receptors. These events were triggered at least in part by activation of the b-catenin pathway. However, unlike maturation induced by microbial products, E-cadherin-stimulated DCs failed to release immunostimulatory cytokines, exhibiting an entirely different transcriptional profile. As a result, E-cadherin-stimulated DCs elicited an entirely different T cell response in vivo, generating T cells with a regulatory as opposed to an effector phenotype. These DCs induced tolerance in vivo and may thus contribute to the elusive steady state tolerogenic DCs.
Publication Title
Disruption of E-cadherin-mediated adhesion induces a functionally distinct pathway of dendritic cell maturation.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 21 Downloadable Samples
- Illumina HumanWG-6 v3.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression.
Sample Metadata Fields
Age, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 21 Downloadable Samples
- Illumina HumanWG-6 v3.0 expression beadchip
Description
We used a genome-wide coding gene expression profiling to identify a gene signature for the molecular classification or prognostic prediction of primary GBMs.
Publication Title
miR-181d: a predictive glioblastoma biomarker that downregulates MGMT expression.
Sample Metadata Fields
Age, Specimen part, Disease, Disease stage
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Ubiquitination-mediated protein degradation of key transcriptional factors is important to the self-renewal of embryonic stem (ES) cells. However, little is known about the deubiquitination in ES self-renewal and differentiation. Here, we report that deubiquitinase USP21 is an important positive regulator to keep ES cells under undifferentiation stasus by deubiquitination and stabilization of Nanog, a key transcriptional factor of ES cells. Loss of USP21 led to ES cells differentiation and defect in reprogramming. Overall design: Gene expression profiles of mouse embryonic stem cell after USP21 knockdown were generated by deep sequencing, using Illumina HighSeq2000, respectively.
Publication Title
The deubiquitinase USP21 maintains the stemness of mouse embryonic stem cells via stabilization of Nanog.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina Genome Analyzer
Description
Nucleosome organization determines chromatin state, which subsequently controls genes expression or silencing. Nucleosome remodeling occurs during somatic cell reprogramming, but it remains undetermined to what degree the re-established nucleosome organization resembles between induced pluripotent stem cells (iPSCs) and embryonic stem cells (ESCs). We generated genome-wide nucleosome maps in mouse ESCs and in iPSCs reprogrammed from somatic cells belonging to three different germ layers using a secondary reprogramming system. Pairwise comparisons showed that the nucleosome organizations in the iPSCs, regardless of the iPSCs¿ tissue of origin, were nearly identical to the ESCs, but distinct to mouse embryonic fibroblasts (MEF). There is a canonical nucleosome arrangement of -1, nucleosome depletion region, +1, +2, +3, et al. nucleosomes around the transcription start sites of active genes whereas only a nucleosome occupies at silent transcriptional units. Transcription factor binding sites possessed characteristic nucleosomal architecture such that their access was governed by the rotational and translational settings of the nucleosome. Interestingly, the tissue-specific genes were highly expressed only in the parental somatic cells of the corresponding iPS cell line before reprogramming, but had a similar expression level in the all resultant iPSCs and ESCs. The re-established nucleosome landscape during nuclear reprogramming provides a conserved setting for accessibility of DNA sequences in mouse pluripotent stem cells. No persistent residual expression program or nucleosome positioning of the parental somatic cells that reflected their tissue of origin were passed onto the resulting mouse iPSCs. Overall design: Gene expression profiles of 5 cell lines with or without biological replicates
Publication Title
Nucleosome organizations in induced pluripotent stem cells reprogrammed from somatic cells belonging to three different germ layers.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Sus scrofa
- 78 Downloadable Samples
- Illumina HiSeq 2500
Description
To optimize the genome annotation, nine tissue and one pool RNA libraries (i.e. heart, liver, spleen, lung, kidney, muscle, fat, ovary, pool.) were constructed using the Illumina mRNA-spleeneq Prep Kit Overall design: We sequenced nine tissues and one pool using illumina Hiseq 2500 platform
Publication Title
Comprehensive variation discovery and recovery of missing sequence in the pig genome using multiple de novo assemblies.
Sample Metadata Fields
Age, Specimen part, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 2000
Description
Mutations in MSX1 cause craniofacial developmental defects, including tooth agenesis, in humans and mice. Previous studies suggest that Msx1 activates Bmp4 expression in the developing tooth mesenchyme to drive early tooth organogenesis. Whereas Msx1-/- mice exhibit developmental arrest of all tooth germs at the bud stage, however, mice with neural crest-specific inactivation of Bmp4 (Bmp4ncko/ncko), which lack Bmp4 expression in the developing tooth mesenchyme, showed developmental arrest of only mandibular molars. We recently demonstrated that deletion of Osr2, which encodes a zinc finger transcription factor expressed in a lingual-to-buccal gradient in the developing tooth bud mesenchyme, rescued molar tooth morphogenesis in both Msx1-/- and Bmp4ncko/ncko mice. In this study, through RNA-seq analyses of the developing tooth mesenchyme in mutant and wildtype embryos, we found that Msx1 and Osr2 have opposite effects on expression of several secreted Wnt antagonists in the tooth bud mesenchyme. Remarkably, both Dkk2 and Sfrp2 exhibit Osr2-dependent preferential expression on the lingual side of the tooth bud mesenchyme and expression of both genes was up-regulated and expanded into the tooth bud mesenchyme in Msx1-/- and Bmp4ncko/ncko mutant embryos. We show that pharmacological activation of canonical Wnt signaling by either lithium chloride (LiCl) treatment or by inhibition of Dkk in utero was sufficient to rescue mandibular molar tooth morphogenesis in Bmp4ncko/ncko mice. Furthermore, whereas inhibition of Dkk alone was insufficient to rescue tooth morphogenesis in Msx1-/- mice, pharmacological inhibition of Dkk in combination with genetic inactivation of Sfrp2 and Sfrp3 rescued maxillary molar morphogenesis in Msx1-/- mice. Together, these data reveal a novel mechanism that the Bmp4-Msx1 pathway drives tooth organogenesis by activating Wnt signaling via regulation of the secreted Wnt antagonists. Overall design: E14 mouse embryos tooth germs were micro-dissceted by LCM, mandibular molar and maxillary molar were seperated, 3 pairs of control and mutant samples were pooled for the RNA extraction
Publication Title
Bmp4-Msx1 signaling and Osr2 control tooth organogenesis through antagonistic regulation of secreted Wnt antagonists.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Mutations in MSX1 cause craniofacial developmental defects, including tooth agenesis, in humans and mice. Previous studies suggest that Msx1 activates Bmp4 expression in the developing tooth mesenchyme to drive early tooth organogenesis. Whereas Msx1-/- mice exhibit developmental arrest of all tooth germs at the bud stage, however, mice with neural crest-specific inactivation of Bmp4 (Bmp4ncko/ncko), which lack Bmp4 expression in the developing tooth mesenchyme, showed developmental arrest of only mandibular molars. We recently demonstrated that deletion of Osr2, which encodes a zinc finger transcription factor expressed in a lingual-to-buccal gradient in the developing tooth bud mesenchyme, rescued molar tooth morphogenesis in both Msx1-/- and Bmp4ncko/ncko mice. In this study, through RNA-seq analyses of the developing tooth mesenchyme in mutant and wildtype embryos, we found that Msx1 and Osr2 have opposite effects on expression of several secreted Wnt antagonists in the tooth bud mesenchyme. Remarkably, both Dkk2 and Sfrp2 exhibit Osr2-dependent preferential expression on the lingual side of the tooth bud mesenchyme and expression of both genes was up-regulated and expanded into the tooth bud mesenchyme in Msx1-/- and Bmp4ncko/ncko mutant embryos. We show that pharmacological activation of canonical Wnt signaling by either lithium chloride (LiCl) treatment or by inhibition of Dkk in utero was sufficient to rescue mandibular molar tooth morphogenesis in Bmp4ncko/ncko mice. Furthermore, whereas inhibition of Dkk alone was insufficient to rescue tooth morphogenesis in Msx1-/- mice, pharmacological inhibition of Dkk in combination with genetic inactivation of Sfrp2 and Sfrp3 rescued maxillary molar morphogenesis in Msx1-/- mice. Together, these data reveal a novel mechanism that the Bmp4-Msx1 pathway drives tooth organogenesis by activating Wnt signaling via regulation of the secreted Wnt antagonists. Overall design: E14.5 mouse embryos tooth germs were micro-dissected by LCM, mandibular molar and maxillary molar were separated, 3 pairs of control and mutant samples were pooled for the RNA extraction. Osr2+/- lower molar and Osr2-/- lower molar.
Publication Title
Bmp4-Msx1 signaling and Osr2 control tooth organogenesis through antagonistic regulation of secreted Wnt antagonists.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples