Evidence map›Paper›PMID 24814285›Full record

ArticleGenome biology and evolution2014

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

Michael J Gaudry, Jay F Storz, Gary Tyler Butts, Kevin L Campbell, Federico G Hoffmann

Open access · goldAbstract read
In one paragraph

Article in Genome biology and evolution, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 30 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Michael J GaudryDepartment of Biological Sciences, University of Manitoba, Winnipeg, MB, Canada.
Jay F StorzSchool of Biological Sciences, University of Nebraska, Lincoln.
Gary Tyler ButtsDepartment of Biochemistry, Molecular Biology, Entomology, and Plant Pathology, Mississippi State University.
Kevin L CampbellDepartment of Biological Sciences, University of Manitoba, Winnipeg, MB, Canada.
Federico G HoffmannDepartment of Biochemistry, Molecular Biology, Entomology, and Plant Pathology, Mississippi State UniversityInstitute for Genomics, Biocomputing and Biotechnology, Mississippi State University federico.g.hoffmann@gmail.com.
Mississippi State University · USUniversity of Manitoba · CAUniversity of Nebraska–Lincoln · US

Funding

Mutational Pleiotropy, Epistasis, and the Adaptive Evolution of Hemoglobin FunctionR01HL087216 · NHLBI · UNIVERSITY OF NEBRASKA LINCOLN · PI STORZ, JAY · 2008 to 2021
$4.5M
NHLBI NIH HHS HL087216-S1NHLBI NIH HHS R01 HL087216
6 · The paper itself

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.

Indexed as

Gene FusionAnimalsbeta-GlobinsChiropteraEvolution, MolecularGene ConversionGene Expression Regulation, DevelopmentalHumansMammalsMultigene FamilyPhylogenybeta-Globinsconcerted evolutiongene conversiongene duplicationgene family evolutionhemoglobinLaurasiatheriaβ-globin

Identifiers

PMID24814285
PMCPMC4041002
OpenAlexW2095928029

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.