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Publication : A highly polymorphic microsatellite in the class II Eb gene allows tracing of major histocompatibility complex evolution in mouse.

First Author  Saha BK Year  1993
Journal  Proc Natl Acad Sci U S A Volume  90
Issue  11 Pages  5312-6
PubMed ID  8506379 Mgi Jnum  J:12570
Mgi Id  MGI:60811 Doi  10.1073/pnas.90.11.5312
Citation  Saha BK, et al. (1993) A highly polymorphic microsatellite in the class II Eb gene allows tracing of major histocompatibility complex evolution in mouse [published erratum appears in Proc Natl Acad Sci U S A 1993 Sep 15;90(18):8757]. Proc Natl Acad Sci U S A 90(11):5312-6
abstractText  A hallmark of major histocompatibility complex (MHC) genes is their extraordinarily high level of polymorphism. Polymorphic residues on MHC molecules determine which peptide ligands they bind and present to effector T lymphocytes. Although the genetic mechanisms responsible for MHC polymorphism have been delineated, the timetable and the pathway of their diversification remain unclear. To trace MHC evolution, we have characterized a highly polymorphic microsatellite containing tandem repeats (TRs) of two tetranucleotide units, TGGA and GGCA, located at the 3' end of the second intron in the class II Eb gene of mouse. On the basis of length as well as sequence variations, 11 TR alleles were defined in 55 inbred mouse strains, which included MHC recombinant haplotypes and haplotypes derived from different subspecies of mouse. In this extensive sampling, a striking concordance was observed between the serologically identified class II proteins and the associated TR alleles. Examination of several strains carrying the same MHC haplotypes as well as strains carrying recombinant MHC haplotypes indicates that TR alleles are extremely stable. These observations suggest that TR polymorphism predates the separation of various subspecies of mouse. On the basis of sequence divergence, a genealogical tree has been constructed to depict evolution of the different TR alleles. Finally, evidence is presented that suggests this microsatellite polymorphism is generated by slipped-strand mispairing during DNA replication.
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