MBE Advance Access published online on September 9, 2008
Molecular Biology and Evolution, doi:10.1093/molbev/msn200
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Research Article |
New Genes Originated via Multiple Recombinational Pathways in the β-Globin Gene Family of Rodents
School of Biological Sciences, University of Nebraska, Lincoln, NE, 68588
1 Current address: Instituto Carlos Chagas – ICC – Fiocruz, Rua Prof. Algacyr Munhoz Mader 3775-CIC, 81350-010, Curitiba, Brazil
2 Current address: Instituto de Ecologia y Evolucion, Facultad de Ciencias, Universidad Austral de Chile, Casilla 567, Valdivia, Chile
Corresponding Author: Jay F. Storz, School of Biological Sciences, University of Nebraska, Lincoln, NE 68588, E-mail: jstorz2{at}unl.edu. Fax: 402/472-2083. Phone: 402/472-1114.
Received for publication July 21, 2008. Revision received August 27, 2008. Accepted for publication September 4, 2008.
Species differences in the size or membership composition of multigene families can be attributed to lineage-specific additions of new genes via duplication, losses of genes via deletion or inactivation, and the creation of chimeric genes via domain shuffling or gene fusion. In principle, it should be possible to infer the recombinational pathways responsible for each of these different types of genomic change by conducting detailed comparative analyses of genomic sequence data. Here we report an attempt to unravel the complex evolutionary history of the β-globin gene family in a taxonomically diverse set of rodent species. The main objectives were 1) to characterize the genomic structure of the β-globin gene cluster of rodents, 2) to assign orthologous and paralogous relationships among duplicate copies of β-like globin genes, and 3) to infer the specific recombinational pathways responsible for gene duplications, gene deletions, and the creation of chimeric fusion genes. Results of our comparative genomic analyses revealed that variation in gene family size among rodent species is mainly attributable to the differential gain and loss of later-expressed β-globin genes via unequal crossing-over. However, two distinct recombinational mechanisms were implicated in the creation of chimeric fusion genes. In muroid rodents, a chimeric
/
fusion gene was created by unequal crossing-over between the embryonic
- and
-globin genes. Interestingly, this
/
fusion gene was generated in the same fashion as the anti-Lepore 5-
-(β/
)-β-3 duplication mutant in humans (the reciprocal exchange product of the pathological hemoglobin Lepore deletion mutant). By contrast, in the house mouse, Mus musculus, a chimeric β/
fusion pseudogene was created by a β-globin
-globin gene conversion event. Although the
/
and β/
fusion genes share a similar chimeric gene structure, they originated via completely different recombinational pathways.
Key Words: chimeric fusion genes gene conversion gene duplication gene family evolution globin genes hemoglobin
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