Skip Navigation

Bioinformatics 2005 21(Suppl 2):ii144-ii150; doi:10.1093/bioinformatics/bti1124
This Article
Right arrow FREE Full Text (Print PDF) Freely available
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 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 (9)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Gabaldón, T.
Right arrow Articles by Huynen, M. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gabaldón, T.
Right arrow Articles by Huynen, M. A.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions{at}oxfordjournals.org

Lineage-specific gene loss following mitochondrial endosymbiosis and its potential for function prediction in eukaryotes

Toni Gabaldón * and Martijn A. Huynen

Center for Molecular and Biomolecular Informatics (CMBI) and Nijmegen Center for Molecular Life Sciences (NCMLS), Radboud University of Nijmegen Medical Center Toernooiveld 1, 6525 ED Nijmegen, the Netherlands

*To whom correspondence should be addressed.

Motivation: The endosymbiotic origin of mitochondria has resulted in a massive horizontal transfer of genetic material from an alpha-proteobacterium to the early eukaryotes. Using large-scale phylogenetic analysis we have previously identified 630 orthologous groups of proteins derived from this event. Here we show that this proto-mitochondrial protein set has undergone extensive lineage-specific gene loss in the eukaryotes, with an average of three losses per orthologous group in a phylogeny of nine species. This gene loss has resulted in a high variability of the alphaproteobacterial-derived gene content of present-day eukaryotic genomes that might reflect functional adaptation to different environments. Proteins functioning in the same biochemical pathway tend to have a similar history of gene loss events, and we use this property to predict functional interactions among proteins in our set.

Contact: T.Gabaldon{at}cmbi.ru.nl

Supplementary information: Sequences and trees for the selected orthologous groups can be accessed at http://www.cmbi.kun.nl/~jagabald/table_groupsb.html


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
 CirculationHome page
M. Benn, M. Schwartz, B. G. Nordestgaard, and A. Tybjaerg-Hansen
Mitochondrial Haplogroups: Ischemic Cardiovascular Disease, Other Diseases, Mortality, and Longevity in the General Population
Circulation, May 13, 2008; 117(19): 2492 - 2501.
[Abstract] [Full Text] [PDF]

Home page
 Genome ResHome page
O. X. Cordero, B. Snel, and P. Hogeweg
Coevolution of gene families in prokaryotes
Genome Res., March 1, 2008; 18(3): 462 - 468.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
T. Gabaldon
Computational approaches for the prediction of protein function in the mitochondrion
Am J Physiol Cell Physiol, December 1, 2006; 291(6): C1121 - C1128.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
C. G. Kurland, L. J. Collins, and D. Penny
Genomics and the irreducible nature of eukaryote cells.
Science, May 19, 2006; 312(5776): 1011 - 1014.
[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.