Skip Navigation



MBE Advance Access published online on June 12, 2007
Molecular Biology and Evolution, doi:10.1093/molbev/msm120
This Article
Right arrow Advance Access manuscript (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
24/9/1912    most recent
msm120v1
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 Gitelman, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gitelman, I.
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

Evolution of the vertebrate twist family and synfunctionalization: a mechanism for differential gene loss through merging of expression domains

Inna Gitelman

Dept. of Virology & Developmental Genetics, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva, 84105, ISRAEL, Tel. 972-8-647-9973 (office); 972-8-647-9956 & 972-8-647-9957 (lab)

email: gitelman{at}bgu.ac.il

Received for publication December 21, 2006. Revision received April 23, 2007. Accepted for publication May 2, 2007.

Twist genes are essential for embryonic development and are conserved from jellyfish to human. To study the vertebrate twist family and its evolution, the entire complement of twist genes was obtained for 9 representative species. Phylogenetic analysis showed that a single protochordate twist gene was duplicated at least twice before the teleost-tetrapod split to give rise to three ancestral genes, which were further duplicated or deleted, resulting in fluctuating number of twist paralogs in different vertebrate lineages. To find whether changes in gene copy number were associated with changes in gene function, embryonic expression patterns of twist orthologs were evaluated against the number of twist paralogs in different species. The results showed evidence for both neo- and subfunctionalization, and, in addition, for loss of an ancestral regulatory gene. For example, in Xenopus, twist2 was lost, but the twist1 paralog acquired, and therefore preserved, twist2 function. A general model is proposed to explain the data. In this process, termed synfunctionalization, one paralog acquires the expression domain(s) of another. The merging may lead to function shuffle. Alternatively, it may leave one paralog redundant and thus subject to deletion - while its function is retained by the surviving paralog(s). Synfunctionalization is a mechanism that, together with neo- and subfunctionalization, may work to establish equilibrium in the number of genes that regulate developmental processes; it may regulate the complexity of regulatory regions as well as gene copy number and therefore may play a role in evolution of gene function and the structure of genome.

Key Words: twist gene expression • synfunctionalization • subfunctionalization • neofunctionalization • gene duplication and loss • function shuffle


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.