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MBE Advance Access published online on March 12, 2009
Molecular Biology and Evolution, doi:10.1093/molbev/msp047
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© 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

Research Article

The NBPF1 Promoter has been Recruited from the Unrelated EVI5 Gene before Simian Radiation

Karl Vandepoele1,2, Vanessa Andries1,2 and Frans van Roy1,2,#

1 Department for Molecular Biomedical Research, VIB, B-9052 Ghent, Belgium
2 Department of Molecular Biology, Ghent University, B-9052 Ghent, Belgium

# To whom correspondence should be addressed: Prof. Dr. Frans van Roy, Department for Molecular Biomedical Research, VIB and Ghent University, Technologiepark 927, B-9052 Ghent (Zwijnaarde), Belgium, E-mail: F.VanRoy{at}DMBR.UGent.be, Fax: +32-9.33.13.500, Tel: +32-9.33.13.604

Received for publication February 7, 2009. Accepted for publication March 2, 2009.

Most new genes arise through the duplication of existing genes. In most cases, the duplication is not limited to the coding sequence but also encompasses the regulatory region. The NBPF gene family has expanded during recent primate evolution, and it has no known mouse ortholog. One of its members, NBPF1, was found to be disrupted by a constitutional translocation in a neuroblastoma patient. Here, we show that the ancestral NBPF gene copied the regulatory region from an unrelated gene, EVI5, after the split between simians and prosimians but before simian radiation. Phylogenetic analysis points to the possible involvement of positive selection acting on the NBPF1 promoter in the simian lineage. We previously showed decreased NBPF1 expression in certain neuroblastoma cell lines. Here, we show that this expression pattern is mimicked by the EVI5 gene, but partly by different mechanisms. Epigenetic regulation of the EVI5 promoter is common in neuroblastoma cell lines, but it is not for the NBPF promoters. Here, we describe the recent acquisition of the NBPF1 promoter from an unrelated gene, and remarkably, both the donor (EVI5) and acceptor (NBPF1) genes are disrupted by constitutional translocations in patients with neuroblastoma, suggesting a functional link between these genes and the disease.

Key Words: NBPF • EVI5 • promoter • duplication


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