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accession-icon GSE37005
Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq
  • organism-icon Mus musculus, Homo sapiens, Saccharomyces cerevisiae
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

Specimen part, Cell line, Treatment

View Samples
accession-icon GSE36958
Gene expression profiles of WT and ime4-/- mutant yeast cells, under vegetative and meiosis-inducing conditions
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Inactivation of the yeast IME4 gene, the yeast homologue of METTL3, was shown to result in the loss of m6A in mRNA of mutant cells grown in sporulation medium. We attempted to characterize the effects of ime4 deletion on gene expression under vegetative and meiosis-inducing conditions. The results show that in vegetatively-growing ime4-/- cells there is an increased expression of the RME1 gene (repressor of meiosis) which prevents precocious entry into the meiotic program. Mutant yeast cells showed reduced expression levels of genes involved in ribosome biogenesis and gene expression processes. Surprisingly, despite the fact that a diploid strain was analyzed, there was also a striking change in the expression level of haploid-specific genes, suggesting that RNA methylation may be used to enforce the sexual identity of diploid cells, required for the implementation of the gametogenesis program. Consistently, when cells were induced to undergo meiosis, ime4-/- diploids failed to undergo the meiotic divisions. Among the genes showing reduced expression in the mutant were IME1 and IME2, the two known inducers of meiosis. Thus, the yeast IME4 gene plays an important role in the regulation of the developmental switch from vegetative cells into gametogenesis.

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP012098
m6A mapping in human RNA (with treatments)
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We developed a novel approach, m6A-seq, for high-resolution mapping of the transcriptome-wide m6A landscape, based on antibody-mediated capture followed by massively parallel sequencing. Overall design: Identification of m6A modified sequences in HepG2 cells. HepG2 cells were incubated with either IFNg (200ng/ml) or HGF/SF (10 ng/ml) over night. Stress effects were tested in HepG2 cells by either 30 minutes incubation at 43ºC (heat shock) or UV irradiation of 0.04 J/cm2 followed by 4 hours of recovery in normal growing conditions prior to harvesting using Trypsin.

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

Cell line, Treatment, Subject

View Samples
accession-icon SRP026084
Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR) [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

Alternative mRNA splicing is a major mechanism for gene regulation and transcriptome diversity. Despite the extent of the phenomenon, the regulation and specificity of the splicing machinery are only partially understood. Adenosine-to-inosine (A-to-I) RNA editing of pre-mRNA by ADAR enzymes has been linked to splicing regulation in several cases. Here we used bioinformatics approaches, RNA-seq and exon-specific microarray of ADAR knockdown cells to globally examine how ADAR and its A-to-I RNA editing activity influence alternative mRNA splicing. Although A-to-I RNA editing only rarely targets canonical splicing acceptor, donor, and branch sites, it was found to affect splicing regulatory elements (SREs) within exons. Cassette exons were found to be significantly enriched with A-to-I RNA editing sites compared with constitutive exons. RNA-seq and exon-specific microarray revealed that ADAR knockdown in hepatocarcinoma and myelogenous leukemia cell lines leads to global changes in gene expression, with hundreds of genes changing their splicing patterns in both cell lines. This global change in splicing pattern cannot be explained by putative editing sites alone. Genes showing significant changes in their splicing pattern are frequently involved in RNA processing and splicing activity. Analysis of recently published RNA-seq data from glioblastoma cell lines showed similar results. Our global analysis reveals that ADAR plays a major role in splicing regulation. Although direct editing of the splicing motifs does occur, we suggest it is not likely to be the primary mechanism for ADAR-mediated regulation of alternative splicing. Rather, this regulation is achieved by modulating trans-acting factors involved in the splicing machinery. Overall design: HepG2 and K562 cell lines were stably transfected with plasmids containing siRNA designed to specifically knock down ADAR expression (ADAR KD). This in order to examine how ADAR affects alternative splicing globally.

Publication Title

Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR).

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE47998
Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR)
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR).

Sample Metadata Fields

Cell line

View Samples
accession-icon SRP012096
METTL3 KD in HepG2 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

To gain insight into possible processes that require m6A for their function, METTL3 was knocked down (KD) in HepG2 cells by siRNA transfections Overall design: Differential expression analysis of METTL3 KD versus mock-transfected HepG2 cells, in 2 biological replicates

Publication Title

Topology of the human and mouse m6A RNA methylomes revealed by m6A-seq.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE47945
Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR) [expression]
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Alternative mRNA splicing is a major mechanism for gene regulation and transcriptome diversity. Despite the extent of the phenomenon, the regulation and specificity of the splicing machinery are only partially understood. Adenosine-to-inosine (A-to-I) RNA editing of pre-mRNA by ADAR enzymes has been linked to splicing regulation in several cases. Here we used bioinformatics approaches, RNA-seq and exon-specific microarray of ADAR knockdown cells to globally examine how ADAR and its A-to-I RNA editing activity influence alternative mRNA splicing. Although A-to-I RNA editing only rarely targets canonical splicing acceptor, donor, and branch sites, it was found to affect splicing regulatory elements (SREs) within exons. Cassette exons were found to be significantly enriched with A-to-I RNA editing sites compared with constitutive exons. RNA-seq and exon-specific microarray revealed that ADAR knockdown in hepatocarcinoma and myelogenous leukemia cell lines leads to global changes in gene expression, with hundreds of genes changing their splicing patterns in both cell lines. This global change in splicing pattern cannot be explained by putative editing sites alone. Genes showing significant changes in their splicing pattern are frequently involved in RNA processing and splicing activity. Analysis of recently published RNA-seq data from glioblastoma cell lines showed similar results. Our global analysis reveals that ADAR plays a major role in splicing regulation. Although direct editing of the splicing motifs does occur, we suggest it is not likely to be the primary mechanism for ADAR-mediated regulation of alternative splicing. Rather, this regulation is achieved by modulating trans-acting factors involved in the splicing machinery.

Publication Title

Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR).

Sample Metadata Fields

Cell line

View Samples
accession-icon GSE45715
Genome-wide analysis of BRCA1 and PALB2
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Genome-wide analysis reveals a role for BRCA1 and PALB2 in transcriptional co-activation.

Sample Metadata Fields

Specimen part, Disease, Cell line

View Samples
accession-icon GSE45713
Genome-wide analysis of BRCA1 and PALB2 [TNF-alpha stimulation]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Breast and ovarian cancer susceptibility genes, BRCA1 and PALB2 have enigmatic roles in cellular growth and mammalian development. While these genes are essential for growth during early developmental programs, inactivation later in adulthood leads to increased growth and formation of tumors, leading to their designation as tumor suppressors. We performed genome-wide analysis assessing their chromatin residence and gene expression responsiveness using high throughput sequencing in breast epithelial cells. These experiments revealed a critical role for BRCA1 and PALB2 in transcriptional responsiveness to NF-kB, a crucial mediator of growth and inflammatory response during development and cancer. Importantly, we also uncovered a vital role for these proteins in response to retinoic acid (RA), a growth inhibitory signal in breast cancer cells, which may constitute the basis for their tumor suppressor activity.

Publication Title

Genome-wide analysis reveals a role for BRCA1 and PALB2 in transcriptional co-activation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE45714
Genome-wide analysis of BRCA1 and PALB2 [RA stimulation]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Breast and ovarian cancer susceptibility genes, BRCA1 and PALB2 have enigmatic roles in cellular growth and mammalian development. While these genes are essential for growth during early developmental programs, inactivation later in adulthood leads to increased growth and formation of tumors, leading to their designation as tumor suppressors. We performed genome-wide analysis assessing their chromatin residence and gene expression responsiveness using high throughput sequencing in breast epithelial cells. These experiments revealed a critical role for BRCA1 and PALB2 in transcriptional responsiveness to NF-kB, a crucial mediator of growth and inflammatory response during development and cancer. Importantly, we also uncovered a vital role for these proteins in response to retinoic acid (RA), a growth inhibitory signal in breast cancer cells, which may constitute the basis for their tumor suppressor activity.

Publication Title

Genome-wide analysis reveals a role for BRCA1 and PALB2 in transcriptional co-activation.

Sample Metadata Fields

Specimen part, Cell line

View Samples
...

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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