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Published September 2012 | Published + Supplemental Material
Journal Article Open

RNA editing in the human ENCODE RNA-seq data


RNA-seq data can be mined for sequence differences relative to the reference genome to identify both genomic SNPs and RNA editing events. We analyzed the long, polyA-selected, unstranded, deeply sequenced RNA-seq data from the ENCODE Project across 14 human cell lines for candidate RNA editing events. On average, 43% of the RNA sequencing variants that are not in dbSNP and are within gene boundaries are A-to-G(I) RNA editing candidates. The vast majority of A-to-G(I) edits are located in introns and 3′ UTRs, with only 123 located in protein-coding sequence. In contrast, the majority of non–A-to-G variants (60%–80%) map near exon boundaries and have the characteristics of splice-mapping artifacts. After filtering out all candidates with evidence of private genomic variation using genome resequencing or ChIP-seq data, we find that up to 85% of the high-confidence RNA variants are A-to-G(I) editing candidates. Genes with A-to-G(I) edits are enriched in Gene Ontology terms involving cell division, viral defense, and translation. The distribution and character of the remaining non–A-to-G variants closely resemble known SNPs. We find no reproducible A-to-G(I) edits that result in nonsynonymous substitutions in all three lymphoblastoid cell lines in our study, unlike RNA editing in the brain. Given that only a fraction of sites are reproducibly edited in multiple cell lines and that we find a stronger association of editing and specific genes suggests that the editing of the transcript is more important than the editing of any individual site.

Additional Information

© 2012, Published by Cold Spring Harbor Laboratory Press. Freely available online through the Genome Research Open Access option. Received November 16, 2011; accepted in revised form May 1, 2012. We thank Wendy Lee and Alicia Rogers for assistance. The work of A.M. and E.P. on this manuscript was supported by the UC Irvine Center for Complex Biological Systems and U.S. National Institutes of Health (NIH) P50 GM076516, and the work of B.W. and B.J.W. was supported by the Beckman Foundation, the Donald Bren Endowment, and NIH grant U54 HG004576.

Attached Files

Published - Genome_Res.-2012-Park-1626-33.pdf

Supplemental Material - SuppFigsS1_S12.pdf

Supplemental Material - SupplementalTable1.txt

Supplemental Material - SupplementalTable10.txt

Supplemental Material - SupplementalTable11.txt

Supplemental Material - SupplementalTable12.txt

Supplemental Material - SupplementalTable13.txt

Supplemental Material - SupplementalTable14.txt

Supplemental Material - SupplementalTable15.txt

Supplemental Material - SupplementalTable16.txt

Supplemental Material - SupplementalTable17.txt

Supplemental Material - SupplementalTable18.txt

Supplemental Material - SupplementalTable19.txt

Supplemental Material - SupplementalTable2.txt

Supplemental Material - SupplementalTable3.txt

Supplemental Material - SupplementalTable4.txt

Supplemental Material - SupplementalTable5.txt

Supplemental Material - SupplementalTable6.txt

Supplemental Material - SupplementalTable7.txt

Supplemental Material - SupplementalTable8.txt

Supplemental Material - SupplementalTable9.txt

Supplemental Material - SupplementaryTable20.xlsx


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August 19, 2023
October 19, 2023