Skip Navigation


Nucleic Acids Research Advance Access originally published online on March 16, 2007
Nucleic Acids Research 2007 35(7):2199-2214; doi:10.1093/nar/gkl1137
This Article
Right arrow Full Text Freely available
Right arrow Print PDF (2761K) Freely available
Right arrow Screen PDF (434K) Freely available
Right arrowOA All Versions of this Article:
35/7/2199    most recent
gkl1137v1
Right arrow Alert me when this article is cited
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 ISI Web of Science
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 (5)
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Heras, S. R.
Right arrow Articles by Thomas, M. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Heras, S. R.
Right arrow Articles by Thomas, M. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2007, Vol. 35, No. 7 2199-2214
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

The L1Tc non-LTR retrotransposon of Trypanosoma cruzi contains an internal RNA-pol II-dependent promoter that strongly activates gene transcription and generates unspliced transcripts

Sara R. Heras, Manuel C. López*, Mónica Olivares and M. Carmen Thomas

Departamento de Biología Molecular, Instituto de Parasitología y Biomedicina ‘López Neyra’, CSIC, 18001 Granada, Spain

*To whom correspondence should be addressed. Tel: +34 958 181 662; Fax: +34 958 181 632; Email: mclopez{at}ipb.csic.es Correspondence may also be addressed to M. Carmen Thomas. Tel: +34 958 181 662; Fax: +34 958 181; Email: mcthomas{at}ipb.csic.es

Received August 30, 2006. Revised December 7, 2006. Accepted December 14, 2006.

L1Tc is the best represented autonomous LINE of the Trypanosoma cruzi genome, throughout which several functional copies may exist. In this study, we show that the first 77 bp of L1Tc (Pr77) (also present in the T. cruzi non-autonomous retrotransposon NARTc, in the Trypanosoma brucei RIME/ingi elements, and in the T. cruzi, T. brucei and Leishmania major degenerate L1Tc/ingi-related elements [DIREs]) behave as a promoter element that activates gene transcription. The transcription rate promoted by Pr77 is 10–14-fold higher than that mediated by sequences located upstream from the T. cruzi tandemly repeated genes KMP11 and the GAPDH. The Pr77 promoter-derived mRNAs initiate at nucleotide +1 of L1Tc, are unspliced and translated. L1Tc transcripts show a moderate half life and are RNA pol II dependent. The presence of an internal promoter at the 5' end of L1Tc favors the production of full-length L1Tc RNAs and reinforces the hypothesis that this mobile element may be naturally autonomous in its transposition.

Present address: Mónica Olivares, PulevaBiotech, Camino Purchil 66, 18004 Granada, Spain


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
 Eukaryot CellHome page
R. T. Souza, M. R. M. Santos, F. M. Lima, N. M. El-Sayed, P. J. Myler, J. C. Ruiz, and J. F. da Silveira
New Trypanosoma cruzi Repeated Element That Shows Site Specificity for Insertion
Eukaryot. Cell, July 1, 2007; 6(7): 1228 - 1238.
[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.