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Arabidopsis thaliana
6 Downloadable Samples
Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Changes ins organellar gene expression trigger retrograde signalling. Prolyl-tRNA synthetase (PRORS1) is located in chloroplasts and mitochondria. Thus, prors1-2 mutants are impaired in chloroplast and mitochondrial gene expression.
Publication Title
Identification of target genes and transcription factors implicated in translation-dependent retrograde signaling in Arabidopsis.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 16 Downloadable Samples
Illumina HiSeq 2000
Description
Homeostasis of the gut microbiota is pivotal to the survival of the host. Intestinal T cells and Innate Lymphoid cells (ILCs) control the composition of the microbiota and respond to its perturbations. Interleukin 22 (IL-22) plays a pivotal role in the immune control of gut commensal and pathogenic bacteria and is secreted by a heterogeneous population of intestinal T cells, NCR- ILC3 and NCR+ILC3. Expression of NCR by ILC3 is believed to define an irreversible effector ILC3 end-state fate in which these cells are key to control of bacterial infection via their production of IL-22. Here we identify the core transcriptional signature that drives the differentiation of NCR- ILC3 into NCR+ ILC3 and reveal that NCR+ILC3 exhibit more plasticity than originally thought, as NCR+ ILC3 can revert to NCR- ILC3. Contrary to the prevailing understanding of NCR+ ILC3 genesis and function, in vivo analyses of mice conditionally deleted of the key ILC3 genes Stat3, Il22, Tbet and Mcl1 demonstrated that NCR+ ILC3 were not essential for the control of colonic infections in the presence of T cells. However, NCR+ ILC3 were mandatory for homeostasis of the caecum. Our data identify that the interplay of intestinal T cells and ILC3 results in robust complementary fail-safe mechanisms that ensure gut homeostasis. Overall design: Transcriptional profiling of wild-type and T-bet knockout innate lymphoid cells (ILC3) using RNA sequencing
Publication Title
Complementarity and redundancy of IL-22-producing innate lymphoid cells.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples
SRP160999- Homo sapiens
- 1 Downloadable Sample
- Illumina HiSeq 3000
Description
Determine mRNA expression levels in cultured cardiomyocytes derived from human iPS cells Overall design: 1 sample
Publication Title
Muscle-specific stress fibers give rise to sarcomeres in cardiomyocytes.
Sample Metadata Fields
Specimen part, Subject
View Samples- Caenorhabditis elegans
- 9 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
Background: The ability of an organism to repair damages to DNA is inextricably linked to aging and cancer. We have characterized and compared the transcriptome of C. elegans mutants deficient in DNA base excision repair, nucleotide excision repair or both to elucidate the transcriptional changes incurred by the reduction of these repair pathways.
Publication Title
A two-tiered compensatory response to loss of DNA repair modulates aging and stress response pathways.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
During adipocyte differentiation, significant alternative splicing changes occur in association with the adipogenic process. However, little is known about roles played by splicing factors in this process. We observed that mice deficient for the splicing factor SRSF10 exhibit severely impaired development of subcutaneous white adipose tissue as a result of defects in adipogenic differentiation. To identify splicing events responsible for this, RNA-seq analysis was performed using embryonic fibroblast cells. Several SRSF10-affected splicing events that are implicated in adipogenesis have been identified. Skipping of lipin1 exon 7 is controlled by SRSF10-regulated cis-element located in the constitutive exon 8. The activity of this element depends on the binding of SRSF10 and correlates with the relative abundance of lipin1a mRNA. A series of experiments demonstrated that SRSF10 controls the production of lipin1a and thus promotes adipocyte differentiation. Indeed, lipin1a expression could rescue SRSF10-mediated adipogenic defects. Taken together, our results identify SRSF10 as an essential regulator for adipocyte differentiation and also provide new insights into splicing control by SRSF10 in lipin1 pre-mRNA splicing. Overall design: RNA-seq for wide type (WT) and SRSF10-deficient (KO) mouse MEF cells
Publication Title
SRSF10 regulates alternative splicing and is required for adipocyte differentiation.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina HiSeq 4000
Description
We report the application of single-cell-based RNA sequencing technology for high-throughput profiling of mice abdominal aortic aneurysm cell type dependent transcriptome. This study provides insight in the expression profile of aortic tissue macrophages in pathological conditions related to cardiovascular diseases. Overall design: Examination of cell specific transcriptomes in three pooled AAA single cell suspensions from three pooled Apolipoprotein deficient mice perfused for 28 days with angiotensin II
Publication Title
Macrophage-derived netrin-1 promotes abdominal aortic aneurysm formation by activating MMP3 in vascular smooth muscle cells.
Sample Metadata Fields
Disease, Treatment, Subject
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling.
Publication Title
Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Genetic susceptibility underlies the pathogenesis of cancer. Through genome-wide association studies, we and others have previously identified a novel susceptibility gene, TNFRSF19, which encodes an orphan member of the TNF receptor superfamily, to be associated with nasopharyngeal carcinoma (NPC) and lung cancer risk. Here, we show that TNFRSF19 is highly expressed in NPC and is required for cell proliferation and NPC development. However, unlike most of TNF receptors, TNFRSF19 is not involved in NF-B activation or associated with TRAF proteins. By affinity purification, we identified TGF receptor type-I (TRI) as a specific binding partner for TNFRSF19. TNFRSF19 binds to the kinase domain of TRI in the cytoplasm and thereby blocks the Smad2/3 association with TRI and subsequent signal transduction. Ectopic expression of TNFRSF19 in normal epithelial cells confers resistance to the cell cycle block induced by TGF, whereas knockout of TNFRSF19 in NPC cells unleashes a potent TGF response characterized by upregulation of Smad2/3 phosphorylation and TGF target gene transcription. Furthermore, elevated TNFRSF19 expression correlates with reduced TGF activity and poor prognosis in NPC patients. Our data reveal that gain-of-function of TNFRSF19 in NPC represents a mechanism by which tumor cells evade the growth-inhibitory action of TGF.
Publication Title
TNFRSF19 Inhibits TGFβ Signaling through Interaction with TGFβ Receptor Type I to Promote Tumorigenesis.
Sample Metadata Fields
Specimen part
View Samples- Macaca mulatta
- 64 Downloadable Samples
- Affymetrix Rhesus Macaque Genome Array (rhesus)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Protection afforded by an HIV vaccine candidate in macaques depends on the dose of SIVmac251 at challenge exposure.
Sample Metadata Fields
Specimen part
View Samples- Macaca mulatta
- 34 Downloadable Samples
- Affymetrix Rhesus Macaque Genome Array (rhesus)
Description
The SIVmac251 macaque model has been used to evaluate the efficacy of vaccine for HIV. Exposure of macaques to a single high dose of SIVmac251 results in transmission of multiple viral variants, which contrasts the few HIV variants typically transmitted in humans. In here, we investigated whether the dose of SIVmac251 challenge affected vaccination efficacy and found that exposure of the immunized macaques to single high dose of SIVmac251 resulted in no vaccine efficacy, whereas exposure to a tenfold lower dose resulted in protection from SIVmac251 acquisition and protection from disease in animals that become infected. The dose of challenge did not affect the expression of inflammatory genes in the gut in acute infection, but at set point, a significant down regulation of interferon responsive genes and up regulation of genes involved in B and T-cell responses, was observed only in vaccinated animals exposed to a lower dose of SIVmac251. Accordingly, in these animals, we also found a significant correlation with vaccine induced T-cell responses and protection from disease. These data demonstrate that the evaluation of the efficacy of vaccine candidates for HIV relies on accurate modeling in macaques to better mimic HIV transmission to humans.
Publication Title
Protection afforded by an HIV vaccine candidate in macaques depends on the dose of SIVmac251 at challenge exposure.
Sample Metadata Fields
Specimen part
View Samples