Comparative Analysis of the α-Like Globin Clusters in Mouse, Rat, and Human Chromosomes Indicates a Mechanism Underlying Breaks in Conserved Synteny

  1. Cristina Tufarelli1,6,
  2. Ross Hardison2,4,
  3. Webb Miller3,4,
  4. Jim Hughes1,
  5. Kevin Clark1,
  6. Nicki Ventress1,
  7. Anna Maria Frischauf5, and
  8. Douglas R. Higgs1,7
  1. 1 MRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK
  2. 2 Department of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, Pennsylvania 16802, USA
  3. 3 Department of Biology, Pennsylvania State University, University Park, Pennsylvania 16802, USA
  4. 4 Huck Institutes of Life Sciences, Pennsylvania State University, University Park, Pennsylvania 16802, USA
  5. 5 Institut fuer Genetik und Allgemeine Biologie, Universitaet Salzburg, A5020 Salzburg, Austria

Abstract

We have sequenced and fully annotated a 65,871-bp region of mouse Chromosome 17 including the Hba-ps4 α-globin pseudogene. Comparative sequence analysis with the functional α-globin loci at human Chromosome 16p13.3 and mouse Chromosome 11 shows that this segment of mouse Chromosome 17 contains a group of three α-like pseudogenes (Hba-psm–Hba-ps4–Hba-q3), similar to the duplicated sets found at the functional mouse cluster on Chromosome 11. In addition, exons 7 to 12 of the mLuc7L gene are present just downstream from the pseudogene cluster, indicating that this clone contains the region in which human 16p13.3 switches in synteny between mouse Chromosomes 11 and 17. Comparison of the sequences around the α-like clusters on the two mouse chromosomes reveals the presence of conserved tandem repeats. We propose that these repetitive elements have played a role in the fragmentation of the mouse α cluster during evolution.

Footnotes

  • [Supplemental material is available online at www.genome.org. The sequence data from this study have been submitted to GenBank/EMBL under accession no. AY016022.]

  • Article and publication are at http://www.genome.org/cgi/doi/10.1101/gr.2143604.

  • ↵6 Present address: Department of Genetics, University of Leicester, Leicester LE1 7RH, UK.

  • ↵7 Corresponding author. E-MAIL doug.higgs{at}imm.ox.ac.uk; FAX 44 1865 222 500.

    • Accepted January 6, 2004.
    • Received November 4, 2003.
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  1. doi: 10.1101/gr.2143604 Genome Res. 14: 623-630 Cold Spring Harbor Laboratory Press

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