Skip Navigation


MBE Advance Access originally published online on June 26, 2009
Molecular Biology and Evolution 2009 26(10):2167-2170; doi:10.1093/molbev/msp127
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary Data
Right arrow All Versions of this Article:
26/10/2167    most recent
msp127v1
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 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 arrowRequest Permissions
Google Scholar
Right arrow Articles by Marco, A.
Right arrow Articles by Marín, I.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Marco, A.
Right arrow Articles by Marín, I.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Letters

CGIN1: A Retroviral Contribution to Mammalian Genomes

Antonio Marco* and Ignacio Marín{dagger}

* Center for Evolutionary Functional Genomics, The Biodesign Institute, Arizona State University
{dagger} Instituto de Biomedicina de Valencia, Consejo Superior de Investigaciones Científicas (IBV-CSIC), Spain

E-mail: imarin{at}ibv.csic.es.

Accepted for publication June 20, 2009.

This study describes the origin and structural features of a mammalian gene, CGIN1 (Cousin of GIN1). CGIN1 proteins contain an NYN domain, retroviral RNase H and integrase domains, and a domain of unknown function (CGIN1 domain) that is also present in two other genes (N4BP1 and KIAA0323). We suggest that CGIN1 derives from the fusion of a KIAA0323-like gene with retroviral sequences, which occurred prior to the marsupial–eutherian split. Sequence and structural analyses indicate that the CGIN1 integrase domain is inactive but still retains the 3D folding observed in retroviral integrases. We hypothesize that CGIN1 may contribute to retroviral resistance in mammals by regulating the ubiquitination of viral proteins.

Key Words: retrovirus • integrase • cooption • viral resistance

Norihiro Okada, Associate Editor


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




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.