Dataset Information

Proteogenomics of adenosine-to-inosine RNA editing in fruit fly

ABSTRACT: This dataset is a part of a bigger work on RNA editing in D. melanogaster brain. We present Orbitrap spectra searched against a customized database of Drosophila proteome with introduction of variants provided by RNA editing. Three files reflect 3 technical replicates.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Drosophila Melanogaster (fruit Fly)

TISSUE(S): Brain

SUBMITTER: Irina Ilina

LAB HEAD: Sergei Moshkovskii

PROVIDER: PXD009590 | Pride | 2018-10-25

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20151203_01_Qp2_DrosophilaBrain_1.mgf	Mgf
	20151203_01_Qp2_DrosophilaBrain_1.mzid	Mzid
	20151203_01_Qp2_DrosophilaBrain_1.raw	Raw
	20151203_02_Qp2_DrosophilaBrain_2.mgf	Mgf
	20151203_02_Qp2_DrosophilaBrain_2.mzid	Mzid

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Publications

Proteogenomics of Adenosine-to-Inosine RNA Editing in the Fruit Fly.

Kuznetsova Ksenia G KG Kliuchnikova Anna A AA Ilina Irina U IU Chernobrovkin Alexey L AL Novikova Svetlana E SE Farafonova Tatyana E TE Karpov Dmitry S DS Ivanov Mark V MV Goncharov Anton O AO Ilgisonis Ekaterina V EV Voronko Olga E OE Nasaev Shamsudin S SS Zgoda Victor G VG Zubarev Roman A RA Gorshkov Mikhail V MV Moshkovskii Sergei A SA

Journal of proteome research 20181017 11

Adenosine-to-inosine RNA editing is one of the most common types of RNA editing, a posttranscriptional modification made by special enzymes. We present a proteomic study on this phenomenon for Drosophila melanogaster. Three proteome data sets were used in the study: two taken from public repository and the third one obtained here. A customized protein sequence database was generated using results of genome-wide adenosine-to-inosine RNA studies and applied for identifying the edited proteins. The ...[more]

PMID: 30298734

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Project description:Adenosine-to-inosine (A-to-I) RNA editing, which is catalyzed by a family of adenosine deaminase acting on RNA (ADAR) enzymes, is important in the epitranscriptomic regulation of RNA metabolism. However, the role of A-to-I RNA editing in vascular disease is unknown. Here we show that cathepsin S mRNA (CTSS), which encodes a cysteine protease associated with angiogenesis and atherosclerosis, is highly edited in human endothelial cells. The 3â?² untranslated region (3â?² UTR) of the CTSS transcript contains two inverted repeats, the AluJo and AluSx+ regions, which form a long stemâ??loop structure that is recognized by ADAR1 as a substrate for editing. RNA editing enables the recruitment of the stabilizing RNA-binding protein human antigen R (HuR; encoded by ELAVL1) to the 3â?² UTR of the CTSS transcript, thereby controlling CTSS mRNA stability and expression. In endothelial cells, ADAR1 overexpression or treatment of cells with hypoxia or with the inflammatory cytokines interferon-Î³ and tumor-necrosis-factor-Î± induces CTSS RNA editing and consequently increases cathepsin S expression. ADAR1 levels and the extent of CTSS RNA editing are associated with changes in cathepsin S levels in patients with atherosclerotic vascular diseases, including subclinical atherosclerosis, coronary artery disease, aortic aneurysms and advanced carotid atherosclerotic disease. These results reveal a previously unrecognized role of RNA editing in gene expression in human atherosclerotic vascular diseases. 1) Evaluation of transcriptome expression and RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in poly(A) RNA-seq data derived from endothelial cell transcriptome after ADAR1 or ADAR2 knockdown (n=2 biological replicates per condition, total n=8 biological samples). 2) Evaluation of transcriptome expression and RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in total-RNA-seq data derived from peripheral blood mononuclear cells (n=12 total biological samples; n=4 replicates per condition). 3) Evaluation of transcriptome expression and RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in total-RNA-seq data derived from endothelial cell transcriptome under basal and hypoxic conditions (n=2 biological replicates per condition, total n=4 biological samples). 4) Evaluation of RNA editing sites (A-to-G and T-to-C nucleotide mismatches) in total RNA-seq data derived from endothelial cell transcriptome under basal and hypoxic conditions after ADAR1 knockdown (n=3 replicates per condition, total n=12 biological samples). 5) HuR iCLIP RNA-sequencing data derived from HUVEC HuR iCLIP after ADAR1 knockdown (scrambled control and siADAR1, n=1 per condition, total n=2 biological samples).