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accession-icon SRP061276
Maize (Zea mays) leaf transcriptome analysis under abiotic stress in wild type and RNA Polymerase IV mutant
  • organism-icon Zea mays
  • sample-icon 29 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Plants have developed complex mechanisms to respond and adapt to abiotic stresses, coupling elaborate modulation of gene expression together with the preservation of genome stability. Epigenetic mechanisms - DNA methylation, chromatin modifications and non coding RNAs - were shown to play a fundamental role in stress-induced gene regulation and may also result in genome destabilization, with the activation and/or the transcription of silenced transposons and retroelements, causing genome rearrangements and novel gene expression patterns. Maize leaf transcriptome was analyzed by total RNA-Seq in both B73 and rmr6 (PolIV mutant involved in siRNA biogenesis and in the RdDM pathway) after drought and salt stress application. Reference annotation based transcript assembly allowed the identification both of new expressed loci and splicing variants, improving the current maize transcriptome annotation. Many antisense transcripts matching on the opposite strand of annotated loci were also identified, while more than the 20% of transcripts represent non coding RNA belonging to four classes: siRNAs, shRNAs, lncRNAs and transposable elements (or their relics). Several lncRNAs are modulated by stress application while TE-related sequences are mainly expressed in rmr6 and up-regulated by the stress. Overall design: Total RNA-Seq analysis of maize leaves from wt and rmr6-1 mutant plants grown under 1) control conditions, 2) drought stress, 3) salt stress, 4) salt+drought stress. Each condition was investigated in triplicate after 10 days of treatment and after 7 days of recovery. Samples derived from replicates 2 and 3 were pooled and sequenced together

Publication Title

Maize RNA PolIV affects the expression of genes with nearby TE insertions and has a genome-wide repressive impact on transcription.

Alternate Accession IDs

GSE71046

Sample Metadata Fields

Treatment, Subject, Time

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accession-icon SRP113797
Control of maize vegetative and reproductive development, fertility and rRNAs silencing by HISTONE DEACETYLASE 108 [PMeA and MiA]
  • organism-icon Zea mays
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Histone deacetylases (HDACs) catalyze the removal of acetyl groups from acetylated histone tails that consequently interact more closely with DNA, leading to chromatin state refractory to transcription. Zea mays HDA108 belongs to the Rpd3/HDA1 HDAC family and is ubiquitously expressed during development. The newly isolated hda108/hda108 insertional mutant exhibited many developmental defects: significant reduction in plant height, alterations of shoot and leaf development, alterations of inflorescence patterning and fertility. Western blot analyses and immunolocalization experiments revealed an evident increase in histone acetylation, accompanied by a marked reduction in H3K9 dimethylation, in mutant nuclei. The DNA methylation status, in the CHG sequence context, and the transcript level of ribosomal sequences were also affected in hda108 mutants, while enrichment in H3 and H4 acetylation characterizes both repetitive and non-repetitive transcriptional up-regulated loci. RNA-Seq both of young leaf and anthers indicated that transcription factor expression is highly affected and that the pollen developmental programme results as disrupted in hda108 mutants. Crosses between hda108/hda108 and epiregulator mutants did not produce any double mutant progeny indicating possible genetic interactions of HDA108 with distinct epigenetic pathways. Our findings indicate that HDA108 is directly involved in regulation of maize development, fertility and epigenetic regulation of genome activity. Overall design: Total RNA-Seq analysis of maize anthers at post-meiotic (PMeA) and mitotic (MiA) stages. 2 biological replicates for stage, each obtained by pooling anthers from three tassels per genotype were collected from wild-type and hda108 mutant plants. Strand-specific sequencing on a Illumina HiSeq2500

Publication Title

Control of Maize Vegetative and Reproductive Development, Fertility, and rRNAs Silencing by <i>HISTONE DEACETYLASE 108</i>.

Alternate Accession IDs

GSE102036

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE73355
The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The goal of this study was to assess whether the presence of HLA-B*35 contributes to activation of ER stress/UPR and inflammation in lcSScPAH PBMC.

Publication Title

The HLA-B*35 allele modulates ER stress, inflammation and proliferation in PBMCs from Limited Cutaneous Systemic Sclerosis patients.

Alternate Accession IDs

E-GEOD-73355

Sample Metadata Fields

Specimen part

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accession-icon GSE71601
Gene and miRNA Expression data from synovium in mouse serum transfer arthritis model (STA) model
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Synovium-Derived MicroRNAs Regulate Bone Pathways in Rheumatoid Arthritis.

Alternate Accession IDs

E-GEOD-71601

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE71599
Gene Expression data from synovium in mouse serum transfer arthritis model (STA) model
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

To find regulated genes during peak inflammation of rheumatoid arthritis (RA), we have collected synovium from mouse Serum Transfer Arthtitis (STA) model at day 0 (Non Arthritic) and day 10 (Peak Inflammation).

Publication Title

Synovium-Derived MicroRNAs Regulate Bone Pathways in Rheumatoid Arthritis.

Alternate Accession IDs

E-GEOD-71599

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE38870
Expression data of satellite cells through muscle injury time course
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Satellite cells are resident skeletal muscle stem cells responsible for muscle maintenance and repair. In resting muscle, satellite cells are maintained in a quiescent state. Satellite cell activation induces the myogenic commitment factor, MyoD, and cell cycle entry to facilitate transition to a population of proliferating myoblasts that eventually exit the cycle and regenerate muscle tissue. The molecular mechanism involved in the transition of a quiescent satellite cell to a transit-amplifying myoblast is poorly understood.

Publication Title

A role for RNA post-transcriptional regulation in satellite cell activation.

Alternate Accession IDs

E-GEOD-38870

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP029172
Implication of small sperm RNAs in the inheritance of the effect of early traumatic stress in mice
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Small non-coding RNAs (sncRNAs) have been proposed as potential vectors of the interface between genes and environment. Here, we report that environmental conditions involving traumatic stress in early life, alter miRNA and piRNA composition in sperm of adult males in mice. Overall design: Examination of small RNA content of sperm from males, that experienced early chronic stress during their first two weeks of life versus small RNA content of sperm from control males.

Publication Title

Implication of sperm RNAs in transgenerational inheritance of the effects of early trauma in mice.

Alternate Accession IDs

GSE50132

Sample Metadata Fields

Sex, Disease, Cell line, Subject

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accession-icon GSE21479
Whole genome sequencing of Saccharomyces cerevisiae: from genotype to phenotype for improved metabolic engineering applications
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

The needs for rapid and efficient microbial cell factory design and construction are possible through the enabling technology, metabolic engineering, which is now being facilitated by systems biology approaches. Metabolic engineering is often complimented by directed evolution, where selective pressure is applied to a partially genetically engineered strain to confer a desirable phenotype. The exact genetic modification or resulting genotype that leads to the improved phenotype is often not identified or understood to enable further metabolic engineering. In this work we establish proof-of-concept that whole genome high-throughput sequencing and annotation can be used to identify single nucleotide polymorphisms (SNPs) between Saccharomyces cerevisiae strains S288c and CEN.PK113-7D. The yeast strain S288c was the first eukaryote sequenced, serving as the reference genome for the Saccharomyces Genome Database, while CEN.PK113-7D is a preferred laboratory strain for industrial biotechnology research. A total of 13,787 high-quality SNPs were detected between both strains (reference strain: S288c). Considering only metabolic genes (782 of 5,873 annotated genes), a total of 219 metabolism specific SNPs are distributed across 158 metabolic genes, with 85 of the SNPs being non-silent (e.g., encoding amino acid modifications). Amongst metabolic SNPs detected, there was pathway enrichment in the galactose uptake pathway (GAL1, GAL10) and ergosterol biosynthetic pathway (ERG8, ERG9). Physiological characterization confirmed a strong deficiency in galactose uptake and metabolism in S288c compared to CEN.PK113-7D, and similarly, ergosterol content in CEN.PK113-7D was significantly higher in both glucose and galactose supplemented cultivations compared to S288c. Furthermore, DNA microarray profiling of S288c and CEN.PK113-7D in both glucose and galactose batch cultures did not provide a clear hypothesis for major phenotypes observed, suggesting that genotype to phenotype correlations are manifested post-transcriptionally or post-translationally either through protein concentration and/or function. With an intensifying need for microbial cell factories that produce a wide array of target compounds, whole genome high-throughput sequencing and annotation for SNP detection can aid in better reducing and defining the metabolic landscape. This work demonstrates direct correlations between genotype and phenotype that provides clear and high-probability of success metabolic engineering targets. The genome sequence, annotation, and a SNP viewer of CEN.PK113-7D are deposited at www.sysbio.se/cenpk.

Publication Title

Whole genome sequencing of Saccharomyces cerevisiae: from genotype to phenotype for improved metabolic engineering applications.

Alternate Accession IDs

E-GEOD-21479

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE18614
Differential Regulation of Mitogen-Activated Protein Kinases by Acetaminophen in TAMH cells
  • organism-icon Mus musculus
  • sample-icon 27 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Acetaminophen (APAP), a widely used analgesic and antipyretic that is considered to be relatively safe at recommended doses, is the leading cause of drug-induced liver failure in the United States. 3-Hydroxyacetanilide (AMAP), a regioisomer of acetaminophen is useful as a comparative tool for studying APAP-induced toxicity since it is non-toxic relative to APAP. TGF-alpha transgenic mouse hepatocytes were treated with both isomers to investigate mitogen-activated protein kinase cascades in order to differentiate their toxicological outcomes. Mitogen-activated protein kinase (MAPK) cascade expression and activation were measured using microarray and Bioplex technologies, respectively. APAP treatment led to c-Jun N-terminal kinase (JNK) activation, whereas AMAP treatment led to the activation of extracellular-signal-regulated protein kinase (ERK). The microarray data suggested APAP treatment may upregulate gene expression at multiple levels of the JNK cascade including a JNK-related scaffold protein. Expression data was related to phosphoprotein levels using the Bioplex system. APAP treatment led to a significant activation of JNK compared to its regioisomer. In contrast, microarray analysis of AMAP showed a slight upregulation of ERK gene activity. Furthermore, Bioplex data showed AMAP treatment led to significant ERK phosphorylation compared to APAP. Cell viability assays confirmed that APAP-induced activation of JNK was related to higher rates of cell death, whereas activation of ERK by AMAP may be cytoprotective.

Publication Title

Differential regulation of mitogen-activated protein kinase pathways by acetaminophen and its nonhepatotoxic regioisomer 3'-hydroxyacetanilide in TAMH cells.

Alternate Accession IDs

E-GEOD-18614

Sample Metadata Fields

Cell line

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accession-icon GSE50382
Effects of neonatal stress and morphine on murine hippocampal gene expression
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Critically ill preterm infants experience multiple stressors while hospitalized. Morphine is commonly prescribed to ameliorate their pain and stress. We hypothesized that neonatal stress will have a dose-dependent effect on hippocampal gene expression, and these effects will be altered by morphine treatment. Male C57BL/6 mice were exposed to 5 treatment conditions between postnatal day 5 and 9: 1) Control, 2) mild stress + saline, 3) mild stress + morphine, 4) severe stress + saline and 5) severe stress + morphine. Hippocampal RNA was extracted and analyzed using Affymetrix Mouse Gene 1.0 ST Arrays. Single gene analysis and gene set analysis were used to compare groups with validation by qPCR. Stress resulted in enrichment of genes sets related to fear response, oxygen carrying capacity and NMDA receptor synthesis. Morphine downregulated gene sets related to immune function. Stress plus morphine resulted in enrichment of mitochondrial electron transport gene sets, and down-regulation of gene sets related to brain development and growth. We conclude that neonatal stress alone influences hippocampal gene expression, morphine alters a subset of stress-related changes in gene expression and influences other gene sets. Stress plus morphine show interaction effects not present with either stimulus alone. These changes may alter neurodevelopment.

Publication Title

Effects of neonatal stress and morphine on murine hippocampal gene expression.

Alternate Accession IDs

E-GEOD-50382

Sample Metadata Fields

Sex, Specimen part, Treatment

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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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