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accession-icon GSE33551
Effects of dietary obesity in fathers on gene expression of fat in the female offspring (mRNA data)
  • organism-icon Rattus norvegicus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

The global prevalence of obesity is increasing across age and gender. The rising burden of obesity in young people contributes to the early emergence of type 2 diabetes. Having one parent obese is an independent risk factor for childhood obesity. While the detrimental impact of diet-induced maternal obesity on offspring is well established, the extent of the contribution of obese fathers is unclear, as is the role of non-genetic factors in the casual pathway. Here we show that paternal high fat diet exposure programmed -cell dysfunction in their F1 female offspring. Chronic high fat diet consumption in Sprague Dawley fathers led to increased body weight, adiposity, impaired glucose tolerance and insulin sensitivity. Relative to controls, their female offspring had lower body weight at day-1, increased pubertal growth rate, impaired insulin secretion and glucose tolerance, in the absence of obesity or increased adiposity. Paternal high fat diet altered the expression of 211 pancreatic islet genes in adult female offspring (P < 0.001); genes belonged to 8 functional clusters, including calcium ion binding, primary metabolic processes and ATP binding, and organ/system development. Broader KEGG pathway analysis of 2014 genes differentially expressed at the P < 0.01 level further demonstrated involvement of insulin and calcium signaling, and MAPK pathways. This is the first reported study in mammals describing non-genetic, intergenerational transmission of metabolic sequelae of high fat diet from father to offspring. These findings support a role of fathers in metabolic programming of offspring and form a framework for further studies.

Publication Title

Paternal high-fat diet consumption induces common changes in the transcriptomes of retroperitoneal adipose and pancreatic islet tissues in female rat offspring.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE33564
Effects of dietary obesity in fathers on gene expression of fat in the female offspring
  • organism-icon Rattus norvegicus
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Paternal high-fat diet consumption induces common changes in the transcriptomes of retroperitoneal adipose and pancreatic islet tissues in female rat offspring.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE27064
Rice endosperm: mRNA profiling and H3K27me3 occupancy
  • organism-icon Oryza sativa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Comparison of four ChIP-Seq analytical algorithms using rice endosperm H3K27 trimethylation profiling data.

Sample Metadata Fields

Specimen part

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accession-icon GSE26840
Express data from rice endosperm
  • organism-icon Oryza sativa
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Immatured rice seeds 7-8 days after pollination were used for expression analysis and matured rice leaf was used as control.

Publication Title

Comparison of four ChIP-Seq analytical algorithms using rice endosperm H3K27 trimethylation profiling data.

Sample Metadata Fields

Specimen part

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accession-icon GSE32719
Expression data from human bone marrow hematopoietic stem cells
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In the human hematopoietic system, aging is associated with decreased bone marrow cellularity, decreased adaptive immune system function, and increased incidence of anemia and other hematological disorders and malignancies. Recent studies in mice suggest that changes within the hematopoietic stem cell (HSC) population during aging contribute significantly to the manifestation of these age-associated hematopoietic pathologies. While the mouse HSC population has been shown to change both quantitatively and functionally with age, changes in the human HSC and progenitor cell populations during aging have not yet been characterized.

Publication Title

Human bone marrow hematopoietic stem cells are increased in frequency and myeloid-biased with age.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE57141
Defining key signaling nodes and therapeutic biomarkers in NF1-mutant cancers
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The NF1 tumor suppressor encodes a RAS GTPase-Activating Protein (RasGAP). Accordingly, deregulated RAS signaling underlies the pathogenesis of NF1-mutant cancers. However, while various RAS effector pathways have been shown to function in these tumors, it is currently unclear which specific proteins within these broad signaling pathways represent optimal therapeutic targets. Here we identify mTORC1 as the key PI3K pathway component in NF1-mutant nervous system malignancies and conversely show that mTORC2 and AKT are dispensable. We also report that combined mTORC1/MEK inhibition is required to promote tumor regression in animal models, but only when the inhibition of both pathways is sustained. Transcriptional profiling studies were also used to establish a predictive signature of effective mTORC1/MEK inhibition in vivo. Within this signature, we unexpectedly found that the glucose transporter gene, GLUT1, was potently suppressed but only when both pathways were effectively inhibited. Moreover, unlike VHL and LKB1 mutant cancers, reduction of 18F-FDG uptake measured by FDG-PET required the effective suppression of both mTORC1 and MEK. Together these studies identify optimal and sub-optimal therapeutic targets in NF1-mutant malignancies and define a non-invasive means of measuring combined mTORC1/MEK inhibition in vivo, which can be readily incorporated into clinical trials.

Publication Title

Defining key signaling nodes and therapeutic biomarkers in NF1-mutant cancers.

Sample Metadata Fields

Specimen part

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accession-icon SRP109837
HPIP controls osteoarthritis cartilage degeneration [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To underly the potential downstream transcriptional regulation of HPIP that could account for cartilage and skeletal development. RNA-seq analysis were performed in HPIP knockout and control primary chondrocytes.Among the 1271 significantly differentially expressed genes, transcripts for 486 (7%) of them were upregulated while transcripts for 785 (11%) were downregulated in HPIP knockout chondrocytes compared to the controls. We found HPIP was closely correlated with the cartilage development. Overall design: Total RNA was isolated with TRIzol from the HPIP knockout and the control primary chondrocytes. Complementary DNA library were prepared and then sequenced by Novel Bioinformatics Co, Ltd (https://en.novogene.com/). Clean reads was obtained from the raw reads by removing the adaptor sequence before read mapping. Reference genome and gene model annotation files were downloaded from genome website browser (NCBI/UCSC/Ensembl). HTSeq V0.6.1 was used to count the read numbers mapped of each gene. And then RPKM of each gene was calculated based on the genes reads count mapped to this gene. Differential expression analysis was performed using the DESeq R package (1.10.1).

Publication Title

Hematopoietic PBX-interacting protein mediates cartilage degeneration during the pathogenesis of osteoarthritis.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE30360
Vreteno, a gonad-specific protein, is essential for germline development and primary piRNA biogenesis in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

In Drosophila, Piwi proteins associate with Piwi-interacting RNAs (piRNAs) and protect the germline genome by silencing mobile genetic elements. This defense system acts in germline and gonadal somatic tissue to preserve germline development. Genetic control for these silencing pathways varies greatly between tissues of the gonad. Here, we identified Vreteno (Vret), a novel gonad-specific protein essential for germline development. Vret is required for piRNA-based transposon regulation in both germline and somatic gonadal tissues. We show that Vret, which contains Tudor domains, associates physically with Piwi and Aubergine (Aub), stabilizing these proteins via a gonad-specific mechanism, absent in other fly tissues. In the absence of vret, Piwi-bound piRNAs are lost without changes in piRNA precursor transcript production, supporting a role for Vret in primary piRNA biogenesis. In the germline, piRNAs can engage in an Aub/Argonaute 3 (AGO3)-dependent amplification in the absence of Vret, suggesting that Vret function can distinguish between primary piRNAs loaded into Piwi/Aub complexes and piRNAs engaged in the amplification cycle. We propose that Vret acts at an early step in primary piRNA processing where it plays an essential role in transposon regulation.

Publication Title

Vreteno, a gonad-specific protein, is essential for germline development and primary piRNA biogenesis in Drosophila.

Sample Metadata Fields

Specimen part, Disease

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accession-icon SRP042020
The exon junction complex controls transposable element activity by ensuring the faithful splicing of the piwi transcript
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The exon junction complex (EJC) is a highly conserved ribonucleoprotein complex which binds RNAs at a late stage of the splicing reaction and remains associated following export to the cytoplasm. This complex is involved in several cellular post-transcriptional processes including mRNA localization, translation and degradation. The EJC plays an additional role in the splicing of a subset of genes in Drosophila and in human cells but the underlying mechanism remains to be elucidated. Here, we have found a novel function for the EJC and its splicing subunit RnpS1 in preventing transposon accumulation in both Drosophila germline and surrounding follicular cells. This function is mediated specifically through the control of the splicing of the piwi transcript. In absence of RnpS1 one of the piwi intron is retained. This intron contains a weak 5’ splice site as well as degenerate transposon fragments, reminiscent of heterochromatic introns. In addition, we identified a small A/T rich region, which alters its polypyrimidine tract (PPT) and confers the RnpS1’s dependency. Finally, we showed that the removal of this intron by RnpS1 requires the initial splicing of the flanking introns, suggesting a model in which the EJC facilitates the splicing of challenging introns following its initial deposition to adjacent exon junctions. Overall design: In total there are 4 different conditions. Comparisons were made between piwi mutant vs control piwi and rnps1 KD vs controls RnpS1

Publication Title

The exon junction complex controls transposable element activity by ensuring faithful splicing of the piwi transcript.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP007339
piRNA production requires heterochromatin formation in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

Here, we analyzed two small RNA libraries derived from ovarian tissue mutant for either the Drosophila SETDB1 gene, or the Bam gene. Here we show that deposition of histone 3 lysine 9 by the methyltransferase dSETDB1 (egg) is required for piRNA cluster transcription. In the absence of dSETDB1, cluster precursor transcription collapses in germline and somatic gonadal cells and TEs are activated, resulting in germline loss and a block in germline stem cell differentiation. We propose that heterochromatin protects the germline by activating the piRNA pathway. Keyword : Epigenetics Overall design: 2 libraries were analyzed, with 1 being a developmental control (Bam Mutant).

Publication Title

piRNA production requires heterochromatin formation in Drosophila.

Sample Metadata Fields

Specimen part, Cell line, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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