Skip Navigation


Bioinformatics Advance Access originally published online on June 5, 2008
Bioinformatics 2008 24(14):1563-1567; doi:10.1093/bioinformatics/btn243
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (Print PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
24/14/1563    most recent
btn243v1
Right arrow Comments: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Comments are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Conley, A. B.
Right arrow Articles by Jordan, I. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Conley, A. B.
Right arrow Articles by Jordan, I. K.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Retroviral promoters in the human genome

Andrew B. Conley , Jittima Piriyapongsa and I. King Jordan *

School of Biology, Georgia Institute of Technology, 310 Ferst Drive, Atlanta, GA 30306, USA

*To whom correspondence should be addressed.


   Abstract

Motivation: Endogenous retrovirus (ERV) elements have been shown to contribute promoter sequences that can initiate transcription of adjacent human genes. However, the extent to which retroviral sequences initiate transcription within the human genome is currently unknown. We analyzed genome sequence and high-throughput expression data to systematically evaluate the presence of retroviral promoters in the human genome.

Results: We report the existence of 51 197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5' untranslated regions (UTRs). A total of 114 of the ERV-derived transcription start sites can be demonstrated to drive transcription of 97 human genes, producing chimeric transcripts that are initiated within ERV long terminal repeat (LTR) sequences and read-through into known gene sequences. ERV promoters drive tissue-specific and lineage-specific patterns of gene expression and contribute to expression divergence between paralogs. These data illustrate the potential of retroviral sequences to regulate human transcription on a large scale consistent with a substantial effect of ERVs on the function and evolution of the human genome.

Contact: king.jordan{at}biology.gatech.edu

Supplementary information: Supplementary data are available at Bioinformatics online.

Associate Editor: John Quackenbush


Received on February 7, 2008; revised on May 19, 2008; accepted on May 20, 2008

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Nucleic Acids ResHome page
A. Levy, S. Schwartz, and G. Ast
Large-scale discovery of insertion hotspots and preferential integration sites of human transposed elements
Nucleic Acids Res., December 14, 2009; (2009) gkp1134v1.
[Abstract] [Full Text] [PDF]


Home page
J. Virol.Home page
U. Schon, O. Diem, L. Leitner, W. H. Gunzburg, D. L. Mager, B. Salmons, and C. Leib-Mosch
Human Endogenous Retroviral Long Terminal Repeat Sequences as Cell Type-Specific Promoters in Retroviral Vectors
J. Virol., December 1, 2009; 83(23): 12643 - 12650.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.