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accession-icon GSE111594
Whole-genome transcriptomic analysis of Notch1-expressing cells in mouse intestinal tumours
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

To define and compare the genome-wide transcriptional signatures of Notch1+ cells in intestinal tumors and in normal ISCs we performed Affymetrix analyses of these two populations.

Publication Title

Lineage tracing of Notch1-expressing cells in intestinal tumours reveals a distinct population of cancer stem cells.

Sample Metadata Fields

Specimen part

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accession-icon SRP042045
Transposon expression kinetics in Dnmt3L-/- developing testes [RNA-seq]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We examined the kinetics of production of mRNAs and small RNAs derived from transposable elements during mouse spermatogenesis, in whole gonads of wildtype and DNA methylation-deficient males (Dnmt3L and Miwi2 mutants). We found that in absence of DNA methylation, transposon reactivation is not constitutive but rather occurs in a class- and development-specific manner : both the intensity of reactivation and the number of reactivated transposon classes increased as germ cells progress in meiosis. Moreover, we observed that transposon silencing before meiosis is not due to increased cleavage by the piRNA machinery. In contrast, the burst of transposon transcripts occurring at meiosis in the absence of DNA methylation serve as substrates for increased piRNA production Overall design: Six whole testis samples were analyzed, corresponding to three time points (16.5dpc, 10dpp and 20dpp) each for Dnamt3L-/- animals and control littermates. For 16.5dpc, testes from 7/8 mice were pooled per genotype. For the other stages, three mice were pooled per genotype.

Publication Title

DNA methylation restrains transposons from adopting a chromatin signature permissive for meiotic recombination.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE54627
Combinatorial flexibility of cytokine during Human T helper cells differentiation
  • organism-icon Homo sapiens
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Transcriptional analysis of human T cells differentiated in 4 T Helper context ( Th0, Th1, Th2 and Th17) in the presence or not of Interferon alpha

Publication Title

Combinatorial flexibility of cytokine function during human T helper cell differentiation.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE57915
The combinatorial code governing cellular responses to complex stimuli
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Integration of multiple signals shapes cell adaptation to their microenvironment through synergistic and antagonistic interactions. The combinatorial complexity governing signal integration for multiple cellular output responses has not been resolved. For outputs measured in the conditions 0 (control), signals X, Y, X+Y, combinatorial analysis revealed 82 possible interaction profiles, which we biologically assimilated to 5 positive, and 5 negative interaction modes. To experimentally validate their use in living cells, we designed an original computational workflow, and applied it to transcriptomics data of innate immune cells integrating physiopathological signal combinations. Up to 9 of the 10 defined modes coexisted in context-dependent proportions. Each integration mode was enriched in specific molecular pathways, suggesting a coupling between genes involved in particular functions, and the corresponding mode of integration. We propose that multimodality and functional coupling are general principles underlying the systems level integration of physiopathological and pharmacological stimuli by mammalian cells.

Publication Title

Combinatorial code governing cellular responses to complex stimuli.

Sample Metadata Fields

Time

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accession-icon SRP017662
Restriction of LINE1 activity by RNAi correlates with mouse ES cell differentiation
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Long interspersed elements 1 (LINE-1 or L1) are retrotransposons that dominate the mouse genomic landscape, and are expressed in Embryonic Stem Cells (ESCs), germ cells, and during early development. Based on clear precedents in plants and fission yeast, we investigated in this study a role for RNAi and other RNA degradation pathways in the regulation of L1 expression and mobilization. We uncovered the existence of novel small (s)RNAs that map to active L1 elements. Some of these sRNAs have characteristics of cognate short-interfering RNA populations, while others display length heterogeneity that evokes a biogenesis through a RNA surveillance pathway, in a Dicer-independent manner. We additionally found that genetic ablation of Dicer and the sRNA effector protein AGO2 has complex and profound consequences on L1 transcription and mobilization in ESCs, indicating that endogenous RNA interference (RNAi) pathway indeed maintain genomic integrity against L1 proliferation. Finally, we investigated the implication of L1 retrotransposition during ESC differentiation and propose that the mobilization of L1 elements in Dicer mutant ESCs could partially explain the inability of these cells to differentiate. Overall design: 2 samples examined: WT E14 and Dicer mutant mouse ESCs

Publication Title

RNAi-dependent and independent control of LINE1 accumulation and mobility in mouse embryonic stem cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP095620
The efficiency of Xist-mediated silencing of X-linked and autosomal genes is determined by the genomic environment
  • organism-icon Mus musculus
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Xist is indispensable for X chromosome inactivation (XCI) in female mammalian cells. However, how Xist RNA directs chromosome-wide transcriptional inactivation of the X chromosome is largely unknown. Here, to study chromosome inactivation by Xist, we generated a system where ectopic Xist expression can be induced from several genomic contexts in aneuploid mouse ES cells. We found that ectopic Xist expression from any location on the X chromosome faithfully recapitulated endogenous XCI, showing the potency of Xist to initiate XCI. Genes that escape XCI remain consistently transcriptionally active upon ectopic XCI, regardless of their position relative to Xist transgenes, and the enrichment of CTCF at their promoters is implicated in directing XCI escape. Xist expression from autosomes facilitates their transcriptional silencing to different degrees, and gene density in proximity of the Xist transcription locus plays a central role in determining the efficiency of gene inactivation. We also show that the enrichment of LINE elements together with a specific chromatin environment facilitates Xist-mediated silencing of both X-linked and autosomal genes. These findings provide new insights into the epigenetic mechanisms that mediate XCI and identify genomic features that promote Xist-mediated chromosome-wide gene inactivation Overall design: 60 RNA-seq from mouse embryonic stem cells and fully differentiated neurons in which ectopic Xist epression is either triggered (plus samples) or not (minus samples) upon doxycycline treatment.

Publication Title

Genetic and epigenetic features direct differential efficiency of Xist-mediated silencing at X-chromosomal and autosomal locations.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

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accession-icon SRP057536
Maternal LSD1/KDM1A is an essential regulator of chromatin and transcription landscapes during zygotic genome activation
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

How the parental genomes of the very specialized sperm and oocyte cells are remodelled upon fertilization to confer totipotency has remained a tantalizing open questions. Indeed, in the case of mammals, the parental genomes undergo dramatic reprogramming upon fertilization, including differential dynamics of histone post-translational modifications. The roles of histone modifying enzymes in this process, which are maternally provided, are only just starting to emerge. Here, we explore the function of the oocyte inherited pool of Lsd1/Kdm1a, which encodes a histone H3K4 and K9 demethylase, during early mouse development. Maternal deficiency of Lsd1/Kdm1a results in developmental arrest by the two-cell stage, associated with dramatic and stepwise alterations in H3K9 and H3K4 methylation patterns depending on its demethylase activity. At the transcriptional level, two major changes occur. On one hand, switch from maternal-to-zygotic program fails to be induced. On the other hand, LINE-1 retrotransposons are not properly silenced, along with evidences for increased LINE-1 activity. We propose that Lsd1/Kdm1a is involved in the correct establishment of epigenetic information harboured by histones and is involved in the initiation of new pattern of genome expression driving early mouse development and preserving genome integrity Overall design: RNA-seq of invidual mouse two-cell stage embryos

Publication Title

Maternal LSD1/KDM1A is an essential regulator of chromatin and transcription landscapes during zygotic genome activation.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP066254
Lsd1 is an essential regulator of the chromatin and transcriptional landscapes during the maternal-to-zygotic
  • organism-icon Mus musculus
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

How the parental genomes of the very specialized sperm and oocyte cells are remodelled upon fertilization to confer totipotency has remained a tantalizing open questions. Indeed, in the case of mammals, the parental genomes undergo dramatic reprogramming upon fertilization, including differential dynamics of histone post-translational modifications. The roles of histone modifying enzymes in this process, which are maternally provided, are only just starting to emerge. Here, we explore the function of the oocyte inherited pool of Lsd1/Kdm1a, which encodes a histone H3K4 and K9 demethylase, during early mouse development. Maternal deficiency of Lsd1/Kdm1a results in developmental arrest by the two-cell stage, associated with dramatic and stepwise alterations in H3K9 and H3K4 methylation patterns depending on its demethylase activity. At the transcriptional level, two major changes occur. On one hand, switch from maternal-to-zygotic program fails to be induced. On the other hand, LINE-1 retrotransposons are not properly silenced, along with evidences for increased LINE-1 activity. We propose that Lsd1/Kdm1a is involved in the correct establishment of epigenetic information harboured by histones and is involved in the initiation of new pattern of genome expression driving early mouse development and preserving genome integrity Overall design: RNA-seq of invidual mouse oocytes

Publication Title

Maternal LSD1/KDM1A is an essential regulator of chromatin and transcription landscapes during zygotic genome activation.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon SRP132194
Differential expression in wild type and mutant HAP1 cells [RNA-seq I]
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

using RNA-seq we characterized gene expression changes occuring upon knockout of BAP1, ASXL1, ASXL2, ASXL1/2 or Polycomb genes RING1B and EZH2. We also investigated the response to retinoic acid treatment in wild-type and BAP1 KO cells. Overall design: Examination of transcript abundance in wild-type HAP1 cells and in 9 different HAP1-mutated cell lines as well as upon retinoic acid treatment in wild-type and BAP1 KO cells. Two biological replicated were performed for each condition.

Publication Title

BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation.

Sample Metadata Fields

Cell line, Treatment, Subject

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accession-icon SRP159677
Differential expression in wild type and mutant HAP1 cells [RNA-seq II]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

Characterization of gene expression changes occuring upon knockout of RING1A, RING1B, and BAP1. Overall design: Four Samples

Publication Title

BAP1 complex promotes transcription by opposing PRC1-mediated H2A ubiquitylation.

Sample Metadata Fields

Specimen part, Treatment, Subject

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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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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