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accession-icon GSE6583
Genome-wide transcriptome analysis of Arabidopsis and siz1-3 response to drought stress
  • organism-icon Arabidopsis thaliana
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)

Description

Post-translational modifications of proteins by Small Ubiquitin-like Modifiers (SUMOs) regulate protein degradation and localization, protein-protein interaction, and transcriptional activity. SUMO E3 ligase functions are executed by SIZ1/SIZ2 in yeast and PIAS family members in human. The Arabidopsis genome contains only one gene, SIZ1, that is orthologous to yeast SIZ1/SIZ2. Here, we show that the Arabidopsis SIZ1 interacts with SUM1 and SCE1a, the SUMO E2 conjugating enzyme. Compared to WT, the null mutant siz-1-3 is smaller in statue because of reduced expression of gene involved in brassinosteroid biosynthesis and signalling. Drought stress induces the accumulation of SUMO-protein conjugates, which is in part dependent on SIZ1 but not on ABA. Mutant plants of siz1-3 have significant lower tolerance to drought stress. Genome wide expression analysis identified about 2,000 Arabidopsis genes that are responsive to drought, and SIZ1 mediates the induction of 600 of these genes by a pathway independent of DREB2A and ABA. SIZ1-dependent, drought-responsive genes include those encoding enzymes of the anthocyanin synthesis pathway and jasmonate response. From these results, we conclude that SIZ1 regulates Arabidopsis development and plays a role in drought stress response probably through the control of gene expression.

Publication Title

The Arabidopsis E3 SUMO ligase SIZ1 regulates plant growth and drought responses.

Alternate Accession IDs

E-GEOD-6583

Sample Metadata Fields

Age

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accession-icon GSE16849
preparative changes in rat intestine and lung for birth
  • organism-icon Rattus norvegicus
  • sample-icon 40 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

To identify genes important in fetal preparation for birth.

Publication Title

Developmental control of the Nlrp6 inflammasome and a substrate, IL-18, in mammalian intestine.

Alternate Accession IDs

E-GEOD-16849

Sample Metadata Fields

Specimen part

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accession-icon SRP015771
Population and sex differences in Drosophila melanogaster brain gene expression
  • organism-icon Drosophila melanogaster
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Background: Changes in gene regulation are thought to be crucial for the adaptation of organisms to their environment. Transcriptome analyses can be used to identify candidate genes for ecological adaptation, but can be complicated by variation in gene expression between tissues, sexes, or individuals. Here we use high-throughput RNA sequencing of a single Drosophila melanogaster tissue to detect brain-specific differences in gene expression between the sexes and between two populations, one from the ancestral species range in sub-Saharan Africa and one from the recently colonized species range in Europe. Results: Relatively few genes (<100) displayed sexually dimorphic expression in the brain, but there was an enrichment of sex-biased genes, especially male-biased genes, on the X chromosome. Over 340 genes differed in brain expression between flies from the African and European populations, with the between-population divergence being highly correlated between males and females. The differentially expressed genes include those involved in stress response, olfaction, and detoxification. Expression differences were associated with transposable element insertions at two genes implicated in insecticide resistance (Cyp6g1 and CHKov1). Conclusions: Analysis of the brain transcriptome revealed many genes differing in expression between populations that were not detected in previous studies using whole flies. There was little evidence for sex-specific regulatory adaptation in the brain, as most expression differences between populations were observed in both males and females. The enrichment of genes with sexually dimorphic expression on the X chromosome is consistent with dosage compensation mechanisms affecting sex-biased expression in somatic tissues. Overall design: mRNA profiles of Drosophila melanogaster brains from adult males and females from a European and an African population (2 biological replicates each)

Publication Title

Population and sex differences in Drosophila melanogaster brain gene expression.

Alternate Accession IDs

GSE40907

Sample Metadata Fields

Sex, Subject

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accession-icon GSE43854
Expression data from primary osteoblasts isolated from calvaria of Gnptab(c.3082insC) knock-in mice compared with osteoblasts isolated from wild-type littermates
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Mucolipidosis type II (MLII) is a severe inherited multisystemic disorder caused by mutations in the GNPTAB gene. Skeletal abnormalities are a predominant feature of MLII. Here we investigate the gene expression in a knock-in mouse model for mucolipidosis type II, generated by the insertion of a cytosine in the murine Gnptab gene (c.3082insC) that is homologous to a homozygous mutation in an MLII patient.

Publication Title

Decreased bone formation and increased osteoclastogenesis cause bone loss in mucolipidosis II.

Alternate Accession IDs

E-GEOD-43854

Sample Metadata Fields

Specimen part

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accession-icon GSE61299
Sharpin controls differentiation and cytokine production of mesenchymal bone marrow cells
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The cytosolic protein Sharpin is as a component of the linear ubiquitin chain assembly complex (LUBAC), which regulates NF-B signaling in response to specific ligands. Its inactivating mutation in Cpdm (chronic proliferative dermatitis mutation) mice causes multi-organ inflammation, yet this phenotype is not transferable into wildtype mice by hematopoietic stem cell transfer. Recent evidence demonstrated that Cpdm mice additionally display low bone mass, but the cellular and molecular causes of this phenotype remained to be established. Here we have applied non-decalcified histology together with cellular and dynamic histomorphometry to perform a thorough skeletal phenotyping of Cpdm mice. We show that Cpdm mice display trabecular and cortical osteopenia, solely explained by impaired bone formation, whereas osteoclastogenesis is unaffected. We additionally found that Cpdm mice display a severe disturbance of articular cartilage integrity in the absence of joint inflammation, supporting the concept that Sharpin-deficiency affects mesenchymal cell differentiation. Consistently, Cpdm mesenchymal cells displayed reduced osteogenic capacitiy ex vivo, yet this defect was not associated with impaired NF-B signaling. A molecular comparison of wildtype and Cpdm bone marrow cell populations further revealed that Cpdm mesenchymal cells produce higher levels of Cxcl5 and lower levels of IL1ra. Collectively, our data demonstrate that skeletal defects of Cpdm mice are not caused by chronic inflammation, but that Sharpin is as a critical regulator of mesenchymal cell differentiation and gene expression. They additionally provide an alternative molecular explanation for the inflammatory phenotype of Cpdm mice and the absence of disease transfer by hematopoetic stem cell transplantation.

Publication Title

Sharpin Controls Osteogenic Differentiation of Mesenchymal Bone Marrow Cells.

Alternate Accession IDs

E-GEOD-61299

Sample Metadata Fields

Specimen part

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accession-icon SRP060292
The LSM1-7 Complex Differentially Regulates Arabidopsis Tolerance to Abiotic Stress Conditions by Promoting Selective mRNA Decapping
  • organism-icon Arabidopsis thaliana
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, Illumina HiSeq 2000

Description

We report the role of LSM1-7 complex in the Arabidopsis tolerance to abiotic stresses. LSM1-7 controls gene expression reprogramming at the post-transcriptional level by promoting the decapping of mRNA. This function is selectively achieve over selected stress-induced transcripts depending on stress nature. Overall design: Comparison of transcriptomes from Col-0 and lsm1a lsm1b plants exposed to low temperatures, drought or high salt conditions

Publication Title

The LSM1-7 Complex Differentially Regulates Arabidopsis Tolerance to Abiotic Stress Conditions by Promoting Selective mRNA Decapping.

Alternate Accession IDs

GSE70491

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP153100
SmE1 is a functional subunit of the Arabidopsis Sm-ring that controls plant development and response to cold stress
  • organism-icon Arabidopsis thaliana
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We report the role of SmE1 protein in the control of Arabidopsis development and tolerance to abiotic stresses. SmE1 controls gene expression reprogramming at the post-transcriptional level by promoting the splicing of pre-mRNA. This function is selectively achieve over selected transcripts depending on the stimulus nature. Overall design: Transcriptomic profiling through RNAseq of Col-0 and sme1-1 plants under control conditions or exposed to low temperatures (4ºC, 24h)

Publication Title

Arabidopsis SME1 Regulates Plant Development and Response to Abiotic Stress by Determining Spliceosome Activity Specificity.

Alternate Accession IDs

GSE116964

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE10527
Genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity
  • organism-icon Rattus norvegicus
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Purpose: Aerobic capacity is a strong predictor of cardiovascular mortality. To determine the relationship between inborn aerobic capacity and soleus gene expression we examined genome-wide gene expression in soleus muscle of rats artificially selected for high and low running capacity (HCR and LCR, respectively) over 16 generations. The artificial selection of LCR caused accumulation of risk factors of cardiovascular disease similar to the metabolic syndrome seen in man, whereas HCR had markedly better cardiac function. We also studied alterations in gene expression in response to exercise training in the two groups, since accumulating evidence indicates that exercise has profound beneficial effects on the metabolic syndrome.

Publication Title

Gene expression profiling of skeletal muscle in exercise-trained and sedentary rats with inborn high and low VO2max.

Alternate Accession IDs

E-GEOD-10527

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE63580
Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells
  • organism-icon Homo sapiens
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells.

Alternate Accession IDs

E-GEOD-63580

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE63552
Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells (Affymetrix)
  • organism-icon Homo sapiens
  • sample-icon 77 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Understanding toxicity pathways of engineered nanomaterials (ENM) has recently been brought forward as a key step in 21st century ENM risk assessment. Molecular mechanisms linked to phenotypic end points is a step towards the development of toxicity tests based on key events, which may allow for grouping of ENM according to their mechanisms of action. This study identified molecular mechanisms underlying mitochondrial dysfunction in human bronchial epithelial BEAS 2B cells following exposure to one of the most studied multi-walled carbon nanotubes (MWCNTs; Mitsui-7). Asbestos was used as a positive control and a non-carcinogenic glass wool material was included as a negative fibre control. Decreased mitochondrial membrane potential (MMP) was observed for MWCNTs at a biologically relevant dose (0.25 g/cm2) and for asbestos at 2 g/cm2, but not for glass wool. Extensive temporal transcriptomic and microRNA expression analyses identified a 330-gene signature related to MWCNT- and asbestos-induced MMP. Fourty-nine of the MMP-associated genes showed highly similar expression patterns over time (six time points) and the majority was found to be regulated by two transcription factors strongly involved in mitochondrial homeostasis, APP and NRF1. In addition, four miRNAs were associated with MMP and one of them, miR-1275, was found to negatively correlate with a large part of the MMP-associated genes. Cellular processes such as gluconeogenesis, glucose metabolism, mitochondrial LC-fatty acid -oxidation and spindle microtubule function were enriched among the MMP-associated genes and miRNAs. These results are expected to be useful in the identification of key events in ENM-related toxicity pathways for the development of molecular screening techniques.

Publication Title

Extensive temporal transcriptome and microRNA analyses identify molecular mechanisms underlying mitochondrial dysfunction induced by multi-walled carbon nanotubes in human lung cells.

Alternate Accession IDs

E-GEOD-63552

Sample Metadata Fields

Specimen part, Treatment

View Samples
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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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Developed by the Childhood Cancer Data Lab

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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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