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Genome Biol Evol. 2014 May 9;6(5):1219-34. doi: 10.1093/gbe/evu097.

Repeated evolution of chimeric fusion genes in the β-globin gene family of laurasiatherian mammals.

Author information

1
Department of Biological Sciences, University of Manitoba, Winnipeg, MB, Canada.
2
School of Biological Sciences, University of Nebraska, Lincoln.
3
Department of Biochemistry, Molecular Biology, Entomology, and Plant Pathology, Mississippi State University.
4
Department of Biochemistry, Molecular Biology, Entomology, and Plant Pathology, Mississippi State UniversityInstitute for Genomics, Biocomputing and Biotechnology, Mississippi State University federico.g.hoffmann@gmail.com.

Abstract

The evolutionary fate of chimeric fusion genes may be strongly influenced by their recombinational mode of origin and the nature of functional divergence between the parental genes. In the β-globin gene family of placental mammals, the two postnatally expressed δ- and β-globin genes (HBD and HBB, respectively) have a propensity for recombinational exchange via gene conversion and unequal crossing-over. In the latter case, there are good reasons to expect differences in retention rates for the reciprocal HBB/HBD and HBD/HBB fusion genes due to thalassemia pathologies associated with the HBD/HBB "Lepore" deletion mutant in humans. Here, we report a comparative genomic analysis of the mammalian β-globin gene cluster, which revealed that chimeric HBB/HBD fusion genes originated independently in four separate lineages of laurasiatherian mammals: Eulipotyphlans (shrews, moles, and hedgehogs), carnivores, microchiropteran bats, and cetaceans. In cases where an independently derived "anti-Lepore" duplication mutant has become fixed, the parental HBD and/or HBB genes have typically been inactivated or deleted, so that the newly created HBB/HBD fusion gene is primarily responsible for synthesizing the β-type subunits of adult and fetal hemoglobin (Hb). Contrary to conventional wisdom that the HBD gene is a vestigial relict that is typically inactivated or expressed at negligible levels, we show that HBD-like genes often encode a substantial fraction (20-100%) of β-chain Hbs in laurasiatherian taxa. Our results indicate that the ascendancy or resuscitation of genes with HBD-like coding sequence requires the secondary acquisition of HBB-like promoter sequence via unequal crossing-over or interparalog gene conversion.

KEYWORDS:

Laurasiatheria; concerted evolution; gene conversion; gene duplication; gene family evolution; hemoglobin; β-globin

PMID:
24814285
PMCID:
PMC4041002
DOI:
10.1093/gbe/evu097
[Indexed for MEDLINE]
Free PMC Article

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