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      Supporting data for characterization of non-coding RNAs associated with the Neuronal growth regulator 1 (NEGR1) adhesion protein

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          Abstract

          Long non-coding RNAs and microRNAs control gene expression to determine central nervous system development and function. Neuronal growth regulator 1 (NEGR1) is a cell adhesion molecule that plays an important role in neurite outgrowth during neuronal development and its precise expression is crucial for correct brain development. The data described here is related to the research article titled “A long non-coding RNA, BC048612 and a microRNA, miR-203 coordinate the gene expression of Neuronal growth regulator 1 (NEGR1) adhesion protein” [1]. This data article contains detailed bioinformatics analysis of genetic signatures at the Negr1 gene locus retrieved from the UCSC genome browser. This approach could be adopted to identify putative regulatory non-coding RNAs in other tissues and diseases.

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          CpG islands in vertebrate genomes.

          M. Gardiner-Garden, M Frommer (1987)
          Although vertebrate DNA is generally depleted in the dinucleotide CpG, it has recently been shown that some vertebrate genes contain CpG islands, regions of DNA with a high G+C content and a high frequency of CpG dinucleotides relative to the bulk genome. In this study, a large number of sequences of vertebrate genes were screened for the presence of CpG islands. Each CpG island was then analysed in terms of length, nucleotide composition, frequency of CpG dinucleotides, and location relative to the transcription unit of the associated gene. CpG islands were associated with the 5' ends of all housekeeping genes and many tissue-specific genes, and with the 3' ends of some tissue-specific genes. A few genes contained both 5' and 3' CpG islands, separated by several thousand base-pairs of CpG-depleted DNA. The 5' CpG islands extended through 5'-flanking DNA, exons and introns, whereas most of the 3' CpG islands appeared to be associated with exons. CpG islands were generally found in the same position relative to the transcription unit of equivalent genes in different species, with some notable exceptions. The locations of G/C boxes, composed of the sequence GGGCGG or its reverse complement CCGCCC, were investigated relative to the location of CpG islands. G/C boxes were found to be rare in CpG-depleted DNA and plentiful in CpG islands, where they occurred in 3' CpG islands, as well as in 5' CpG islands associated with tissue-specific and housekeeping genes. G/C boxes were located both upstream and downstream from the transcription start site of genes with 5' CpG islands. Thus, G/C boxes appeared to be a feature of CpG islands in general, rather than a feature of the promoter region of housekeeping genes. Two theories for the maintenance of a high frequency of CpG dinucleotides in CpG islands were tested: that CpG islands in methylated genomes are maintained, despite a tendency for 5mCpG to mutate by deamination to TpG+CpA, by the structural stability of a high G+C content alone, and that CpG islands associated with exons result from some selective importance of the arginine codon CGX. Neither of these theories could account for the distribution of CpG dinucleotides in the sequences analysed. Possible functions of CpG islands in transcriptional and post-transcriptional regulation of gene expression were discussed, and were related to theories for the maintenance of CpG islands as "methylation-free zones" in germline DNA.
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            Transcriptome analysis by strand-specific sequencing of complementary DNA

            D Parkhomchuk, T Borodina, V. Amstislavskiy … (2009)
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              A reference methylome database and analysis pipeline to facilitate integrative and comparative epigenomics

              Q Song, B Decato, E Hong … (2013)
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                Author and article information

                Contributors
                Kandiah Jeyaseelan
                Journal
                Journal ID (nlm-ta): Data Brief
                Journal ID (iso-abbrev): Data Brief
                Title: Data in Brief
                Publisher: Elsevier
                ISSN (Electronic): 2352-3409
                Publication date PMC-release: 27 February 2016
                Publication date Collection: June 2016
                Publication date (Electronic): 27 February 2016
                Volume: 7
                Pages: 381-385
                Affiliations
                [a ]Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 8 Medical Drive, 117597 Singapore
                [b ]Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, 10 Medical Drive, 117597 Singapore
                [c ]Department of Anatomy and Developmental Biology, School of Biomedical Sciences, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria 3800, Australia
                Author notes
                [* ]Corresponding author at: Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 8 Medical Drive, 117597 Singapore. Tel.: +65 65163248. bchjeya@ 123456nus.edu.sg
                Article
                Publisher ID: S2352-3409(16)30075-0
                DOI: 10.1016/j.dib.2016.02.053
                PMC ID: 4781925
                PubMed ID: 26977442
                SO-VID: 5111582e-f5cf-429f-83cc-941f836f94d9
                Copyright © © 2016 Published by Elsevier Inc.
                License:

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 29 December 2015
                Date revision received : 27 January 2016
                Date accepted : 19 February 2016
                Categories
                Subject: Data Article

                Keywords: bioinformatics,long non-coding rna,microrna,negr1,regulation
                Data availability:
                Keywords: bioinformatics, long non-coding rna, microrna, negr1, regulation

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