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Series GSE47997 Query DataSets for GSE47997
Status Public on Jun 17, 2013
Title Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR) [RNA-seq]
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary 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.
Contributor(s) Solomon O, Oren S, Safran M, Deshet-Unger N, Akiva P, Jacob-Hirsch J, Cesarkas K, Kabesa R, Amariglio N, Unger R, Rechavi G, Eyal E
Citation(s) 23474544
Submission date Jun 17, 2013
Last update date Oct 25, 2022
Contact name jasmine Jacob
Phone 0523790500
Organization name Sheba Medical Center at Tel HaShomer
Street address haChevel 33
City Shoham
State/province -Select-
ZIP/Postal code 60850
Country Israel
Platforms (1)
GPL10999 Illumina Genome Analyzer IIx (Homo sapiens)
Samples (4)
GSM1164649 HepG2_control
GSM1164650 HepG2_ADARkd
GSM1164651 K562_control
This SubSeries is part of SuperSeries:
GSE47998 Global regulation of alternative splicing by adenosine deaminase acting on RNA (ADAR)
BioProject PRJNA208620
SRA SRP026084

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Supplementary file Size Download File type/resource
GSE47997_HepG2_AS_regions.xls.gz 4.3 Mb (ftp)(http) XLS
GSE47997_HepG2_DE_2_fold.xls.gz 87.0 Kb (ftp)(http) XLS
GSE47997_K562_AS_regions.xls.gz 4.5 Mb (ftp)(http) XLS
GSE47997_K562_DE_2_fold.xls.gz 51.4 Kb (ftp)(http) XLS
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Raw data are available in SRA
Processed data are available on Series record

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