Structure of the MHC A and B locus promoters in hominoids: Insights on the evolution of the class I MHC multigene family

Abbe N. Vallejo, Larry R Pease

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The expansion and contraction of mammalian class I multigene families raises the issue as to what determines the loss or retention of family members. We propose that accumulating changes in regulatory regions result in the loss of expression of the gene products during times critical to selection, leading to the extinction of misregulated genes. The structures of promoter regions of MHC class I genes in nonhuman primates support this view. The B promoters are more homogeneous and contain regulatory elements also found in the promoters of the homologous class I genes of more distant mammals, whereas the A locus promoters were significantly more heterogeneous, have fewer sequence motifs related to known transcription factor-binding sites and have accumulated nucleotide substitutions within one of the widely conserved class I promoter elements. These findings are consistent with the view that the more polymorphic B locus is the principal MHC locus encoding functional class I Ag-presenting molecules whereas the less polymorphic A locus is assuming a secondary role as a consequence of promoter defects.

Original languageEnglish (US)
Pages (from-to)3922-3931
Number of pages10
JournalJournal of Immunology
Volume154
Issue number8
StatePublished - 1995

Fingerprint

MHC Class I Genes
Multigene Family
Nucleic Acid Regulatory Sequences
Genetic Promoter Regions
Primates
Mammals
Transcription Factors
Nucleotides
Binding Sites
Gene Expression
Genes
Retention (Psychology)
Psychological Extinction

ASJC Scopus subject areas

  • Immunology

Cite this

Structure of the MHC A and B locus promoters in hominoids : Insights on the evolution of the class I MHC multigene family. / Vallejo, Abbe N.; Pease, Larry R.

In: Journal of Immunology, Vol. 154, No. 8, 1995, p. 3922-3931.

Research output: Contribution to journalArticle

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