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dc.contributor.authorAlam, Tanvir
dc.contributor.authorMedvedeva, Yulia
dc.contributor.authorJia, Hui
dc.contributor.authorBrown, James B.
dc.contributor.authorLipovich, Leonard
dc.contributor.authorBajic, Vladimir B.
dc.date.accessioned2014-11-16T08:31:09Z
dc.date.available2014-11-16T08:31:09Z
dc.date.issued2014-10-02
dc.identifier.citationAlam T, Medvedeva YA, Jia H, Brown JB, Lipovich L, et al. (2014) Promoter Analysis Reveals Globally Differential Regulation of Human Long Non-Coding RNA and Protein-Coding Genes. PLoS ONE 9(10): e109443. doi:10.1371/journal.pone.0109443
dc.identifier.issn1932-6203
dc.identifier.pmid25275320
dc.identifier.doi10.1371/journal.pone.0109443
dc.identifier.urihttp://hdl.handle.net/10754/334972
dc.description.abstractTranscriptional regulation of protein-coding genes is increasingly well-understood on a global scale, yet no comparable information exists for long non-coding RNA (lncRNA) genes, which were recently recognized to be as numerous as protein-coding genes in mammalian genomes. We performed a genome-wide comparative analysis of the promoters of human lncRNA and protein-coding genes, finding global differences in specific genetic and epigenetic features relevant to transcriptional regulation. These two groups of genes are hence subject to separate transcriptional regulatory programs, including distinct transcription factor (TF) proteins that significantly favor lncRNA, rather than coding-gene, promoters. We report a specific signature of promoter-proximal transcriptional regulation of lncRNA genes, including several distinct transcription factor binding sites (TFBS). Experimental DNase I hypersensitive site profiles are consistent with active configurations of these lncRNA TFBS sets in diverse human cell types. TFBS ChIP-seq datasets confirm the binding events that we predicted using computational approaches for a subset of factors. For several TFs known to be directly regulated by lncRNAs, we find that their putative TFBSs are enriched at lncRNA promoters, suggesting that the TFs and the lncRNAs may participate in a bidirectional feedback loop regulatory network. Accordingly, cells may be able to modulate lncRNA expression levels independently of mRNA levels via distinct regulatory pathways. Our results also raise the possibility that, given the historical reliance on protein-coding gene catalogs to define the chromatin states of active promoters, a revision of these chromatin signature profiles to incorporate expressed lncRNA genes is warranted in the future.
dc.description.sponsorshipTA and VBB were supported by KAUST Base Research Fund to VBB. LL was supported by the ENCODE Consortium through NIH 1U01-HG007031 to Peter Bickel, University of California, Berkeley. JBB's work was supported by NHGRI K99 HG006698. HJ was supported by the Wayne State University Perinatal Initiative. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
dc.language.isoen
dc.publisherPublic Library of Science (PLoS)
dc.relation.urlhttp://dx.plos.org/10.1371/journal.pone.0109443
dc.rightsThis is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectChromatin
dc.subjectDNA methylation
dc.subjectDNA transcription
dc.subjectGene expression
dc.subjectGene regulation
dc.subjectLong non-coding RNAs
dc.subjectSequence motif analysis
dc.subjectTranscription factors
dc.titlePromoter Analysis Reveals Globally Differential Regulation of Human Long Non-Coding RNA and Protein-Coding Genes
dc.typeArticle
dc.contributor.departmentApplied Mathematics and Computational Science Program
dc.contributor.departmentComputational Bioscience Research Center (CBRC)
dc.contributor.departmentComputer Science Program
dc.contributor.departmentComputer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
dc.identifier.journalPLoS ONE
dc.identifier.pmcidPMC4183604
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, Michigan, United States of America
dc.contributor.institutionDepartment of Genome Dynamics, Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, United States of America
dc.contributor.institutionDepartment of Neurology, School of Medicine, Wayne State University, Detroit, Michigan, United States of America
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)
kaust.personAlam, Tanvir
kaust.personMedvedeva, Yulia
kaust.personBajic, Vladimir B.
refterms.dateFOA2018-06-13T16:03:26Z


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This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.