Skip Navigation



MBE Advance Access published online on June 30, 2007
Molecular Biology and Evolution, doi:10.1093/molbev/msm130
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
24/9/2009    most recent
msm130v1
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 Ichiyanagi, K.
Right arrow Articles by Okada, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ichiyanagi, K.
Right arrow Articles by Okada, N.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. 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

Research Article

Acquisition of Endonuclease Specificity During Evolution of L1 Retrotransposon

Kenji Ichiyanagi1,3, Hidenori Nishihara1, David D. Duvernell2 and Norihiro Okada1,4

1 Department of Biological Sciences, Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259-B21 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan
2 Department of Biological Sciences, Southern Illinois University, Edwardsville, IL 62026, USA
3 present address: Division of Human Genetics, Department of Integrated Genetics, National Institute of Genetics, 1111 Yata, Mishima, Shizuoka 411-8540, Japan

4 Corresponding author: Norihiro Okada email: nokada{at}bio.titech.ac.jp phone: 45-924-5742 fax: 45-924-5835

Accepted for publication June 20, 2007.

L1 is the most proliferative autonomous retroelement that comprises about 20% of mammalian genomes. Why L1s have proliferated so extensively in mammalian genomes is an important yet unsolved question. L1 copies are amplified via retrotransposition, in which the DNA cleavage specificity by the L1-encoded endonuclease (EN) primarily dictates sites of insertion. Whereas mammalian L1s show target preference for 5'-TTAAAA-3', other L1-like elements exhibit various degrees of target specificity. To gain insights on diversification of the EN specificity during L1 evolution, ENs of zebrafish L1 elements were analyzed here. We revealed that they form three discrete clades, M, F, and Tx1, which is in stark contrast to a single L1 clade in mammalian species. Interestingly, zebrafish clade M elements cluster as a sister group of mammalian L1s and show target-site preference for 5'-TTAAAA-3'. In contrast, elements of the clade F, the immediate outgroup of the clade M, show little specificity. We identified certain clade-specific amino acid residues in EN, many of which are located in the cleft that recognizes the substrate, suggesting that these amino acid alterations have generated two types of ENs with different substrate specificities. The distribution pattern of the three clades suggests a possibility that the acquisition of target specificity by the L1 ENs improved the L1 fitness under the circumstances in mammalian hosts.

Key Words: cleavage specificity • endonuclease • L1 evolution • LINE • retrotransposon


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
 Mol Biol EvolHome page
K. Ichiyanagi and N. Okada
Mobility Pathways for Vertebrate L1, L2, CR1, and RTE Clade Retrotransposons
Mol. Biol. Evol., June 1, 2008; 25(6): 1148 - 1157.
[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.