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accession-icon SRP131067
Roles of the Brca2 and Wapl complexes with Pds5 in sister chromatid cohesion, cohesin localization, and gene expression [RNA-seq]
  • organism-icon Drosophila melanogaster
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

RNA expression was measured by RNA-seq in Drosophila ML-DmBG3-c2 cells depleted for proteins involved in sister chromatid cohesion, and in developing third instar wing discs with or withough brca2 gene mutations Overall design: RNA expression in depleted cells was compared to mock treated cells and RNA expression in wing discs from brca2 mutant Drosophila was compared to expression in wing discs without brca2 mutations This series includes mock RNAi treated samples re-used from GSE100547.

Publication Title

Brca2, Pds5 and Wapl differentially control cohesin chromosome association and function.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP110597
Polycomb Repressive Complex 1 regulates transcription of active genes [RNAseq]
  • organism-icon Drosophila melanogaster
  • sample-icon 14 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

RNA expression was measured using RNA-seq Overall design: RNA levels in Mock-treated control Drosophila cells were compared to RNA levels in cells RNAi depleted for Ph, Sce, and Pc

Publication Title

Polycomb repressive complex 1 modifies transcription of active genes.

Sample Metadata Fields

Subject

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accession-icon SRP110596
Polycomb Repressive Complex 1 regulates transcription of active genes [NTseq]
  • organism-icon Drosophila melanogaster
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

RNA nascent transcription was measured using NT-seq Overall design: RNA nascent transcript levels in Mock-treated control Drosophila cells were compared to those in cells RNAi depleted for Ph and Sce

Publication Title

Polycomb repressive complex 1 modifies transcription of active genes.

Sample Metadata Fields

Subject

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accession-icon GSE42106
Cohesin and Polycomb proteins functionally interact to control transcription at silenced, restrained, and active genes
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Cohesin and polycomb proteins functionally interact to control transcription at silenced and active genes.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE42105
Cohesin and Polycomb proteins functionally interact to control transcription at silenced, restrained, and active genes [expression array data]
  • organism-icon Drosophila melanogaster
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Cohesin is crucial for proper chromosome segregation, but also regulates gene transcription and organism development by poorly understood mechanisms. We find that in Drosophila, cohesin functionally interacts with Polycomb group (PcG) silencing proteins at both silenced and active genes. Cohesin unexpectedly facilitates binding of Polycomb Repressive Complex 1 (PRC1) to many active genes. In contrast, cohesin and PRC1 binding are mutually antagonistic at silenced genes. PRC1 depletion decreases phosphorylated RNA polymerase and mRNA at many active genes, but increases them at silenced genes. Cohesin also facilitates long-range interactions between Polycomb Response Elements in the invected-engrailed gene complex where it represses transcription. These multiple distinct cohesin-PcG interactions reveal a previously unrecognized role for PRC1 in facilitating productive gene transcription, and provide new insights into how cohesin and PRC1 control development.

Publication Title

Cohesin and polycomb proteins functionally interact to control transcription at silenced and active genes.

Sample Metadata Fields

Sex

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accession-icon GSE18795
Expression data from zebrafish embryos homozygous mutant for the cohesin subunit Rad21
  • organism-icon Danio rerio
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Zebrafish Genome Array (zebrafish)

Description

Rad21 is a subunit of cohesin. The main function of cohesin is to hold replicated chromosomes together until cells divide, but it also plays a role in gene expression. To find out which genes might be regulated by cohesin, a study was conducted to look for global changes in gene expression in zebrafish embryos lacking cohesin component Rad21.

Publication Title

Positive regulation of c-Myc by cohesin is direct, and evolutionarily conserved.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE16152
Effects of Nipped-B and Rad21 sister chromatid cohesin proteins on gene expression in Drosophila ML-DmBG3 cells
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Drosophila Genome 2.0 Array (drosophila2)

Description

Effects of Nipped-B and Rad21 sister chromatid cohesin proteins on gene expression data in ML-DmBG3 cells derived from Drosophila melanogaster larval central nervous system

Publication Title

Regulation of the Drosophila Enhancer of split and invected-engrailed gene complexes by sister chromatid cohesion proteins.

Sample Metadata Fields

Time

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accession-icon SRP017251
Genome-wide control of RNA polymerase II activity by cohesin (sequencing)
  • organism-icon Drosophila melanogaster
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Cohesin is a well-known mediator of sister chromatid cohesion, but it also influences gene expression and development. These non-canonical roles of cohesin are not well understood, but are vital: gene expression and development are altered by modest changes in cohesin function that do not disrupt chromatid cohesion. To clarify cohesin’s roles in transcription, we measured how cohesin controls RNA polymerase II (Pol II) activity by genome-wide chromatin immunoprecipitation and precision global run-on sequencing. On average, cohesin-binding genes have more transcriptionally active Pol II and promoter-proximal Pol II pausing than non-binding genes, and are more efficient, producing higher steady state levels of mRNA per transcribing Pol II complex. Cohesin depletion frequently increases pausing at cohesin-binding genes, indicating that cohesin often facilitates transition of paused Pol II to elongation. In many cases this likely reflects a role for cohesin in transcriptional enhancer function. Strikingly, more than 95% of predicted extragenic enhancers bind cohesin, and cohesin depletion can reduce their association with Pol II, indicating that cohesin facilitates enhancer-promoter contact. Cohesin directly promotes transcription of the myc gene, and cohesin depletion reduces Pol II activity at most Myc target genes. The multiple transcriptional roles of cohesin revealed by these studies likely underlie the growth and developmental deficits caused by minor changes in cohesin activity. Overall design: The PRO-seq method was used to measure transcriptionally engaged Pol II genome-wide in two replicates each of mock RNAi-treated, Nipped-B RNAi-treated, and Rad21 RNAi-treated ML-DmBG3-c2 cells.

Publication Title

Genome-wide control of RNA polymerase II activity by cohesin.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject

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accession-icon GSE64034
Transcriptome comparison between CHOPS syndrome and Cornelia de Lange syndrome
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

CHOPS syndrome is caused by germline gain-of-function mutations of AFF4. Cornelia de Lange syndrome is caused by germline mutations of cohesin loading factors or cohesin complex genes such as NIPBL, SMC1A, SMC3 and HDAC8. There are many overlapping clinical features exist between CHOPS syndrome and Cornelia de Lange syndrome. To identified commonly dysregulated genes in CHOPS syndrome and Cornelia de Lange syndrome, we perfomred side-by-side transcriptome comparison between CHOPS syndrome and Cornelia de Lange syndrome.

Publication Title

Germline gain-of-function mutations in AFF4 cause a developmental syndrome functionally linking the super elongation complex and cohesin.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE64031
Transcriptome characterization of CHOPS syndrome, a novel genetic disorder caused by gain-of-function mutations of AFF4
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

AFF4 is a component of super elongation complex (SEC), which plays an important role in mobilizing paused RNA polymerase II at gene promoter regions. Using exome sequenging, we have identified a novel genetic disorder caused by missense mutations in AFF4. We propose CHOPS syndrome as a name for this new diagnosis. To evaluate the effect of identified missense mutations of AFF4, utilizing patient derived skin fibroblast cell lines, the gene expression analysis was perfomred.

Publication Title

Germline gain-of-function mutations in AFF4 cause a developmental syndrome functionally linking the super elongation complex and cohesin.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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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