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Comparative Analysis of the α-Like Globin Clusters in Mouse, Rat, and Human Chromosomes Indicates a Mechanism Underlying Breaks in Conserved Synteny
Author(s) -
Cristina Tufarelli,
Ross C. Hardison,
Webb Miller,
Jim R. Hughes,
Kevin Clark,
Nicki Ventress,
A.-M. Frischauf,
Douglas R. Higgs
Publication year - 2004
Publication title -
genome research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 9.556
H-Index - 297
eISSN - 1549-5469
pISSN - 1088-9051
DOI - 10.1101/gr.2143604
Subject(s) - biology , pseudogene , synteny , genetics , chromosome 15 , chromosome 17 (human) , chromosome 16 , chromosome 21 , gene cluster , chromosome 22 , globin , chromosome , gene , chromosome 19 , chromosome regions , microbiology and biotechnology , genome
We have sequenced and fully annotated a 65,871-bp region of mouse Chromosome 17 including the Hba-ps4 alpha-globin pseudogene. Comparative sequence analysis with the functional alpha-globin loci at human Chromosome 16p13.3 and mouse Chromosome 11 shows that this segment of mouse Chromosome 17 contains a group of three alpha-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 alpha-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 alpha cluster during evolution.

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