| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Structural Biology, and Department of Microbiology and Immunology, School of Medicine, Stanford University, Stanford, CA 94305
Orangutan (Pongo pygmaeus) MHC-C appears less evolved than human HLA-C: Popy-C is not fixed and its alleles encode only one (C1) of the two motifs for killer cell Ig-like receptor (KIR) ligands. To assess the structure and complexity of the orangutan KIR locus, the complete nucleotide sequence of an orangutan KIR haplotype was determined. The PopyKIR locus is flanked by LILR and FCAR and consists of seven genes and pseudogenes, two novel and five corresponding to known cDNA. Distinguishing all KIRs in this rapidly evolving KIR locus from the KIR3DX1 gene is an LTR33A/MLT1D element in intron 3. These two forms of KIR represent lineages that originated by duplication of a common ancestor. The conserved, framework regions of primate KIR loci comprise the 5' part of a lineage V KIR, the 3' part of a pseudogene, the complete 2DL4 gene, and the 3' part of a lineage II KIR. Although previously defined PopyKIR2DL4 alleles contain premature termination codons, the sequenced haplotype’s PopyKIR2DL4 allele encodes a full-length protein. A model for KIR evolution is proposed. Distinguishing the orangutan KIR haplotype from the proposed common ancestor of primate KIR haplotypes is an increased number to give three lineage III KIR genes in the centromeric part of the locus, the site for most human lineage III genes encoding HLA-C specific KIR. Thus, expansion of lineage III KIR is associated with emergence of MHC-C.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grants AI031168 and AI024258 (to P.P.) and a Ruth L. Kirschstein National Research Service Award (F30) from National Institutes of Health (to A.M.O.A.).
2 Address correspondence and reprint requests to Dr. Peter Parham, Department of Structural Biology, Stanford University, Fairchild D-159, 299 Campus Drive West, Stanford, CA 94305. E-mail address: peropa{at}stanford.edu
3 Abbreviations used in this paper: KIR, killer cell Ig-like receptor; NJ, neighbor joining; mya, million years ago; LRC, leukocyte receptor complex; LINE, long interspersed nuclear element; dN, rate of nonsynonymous substitution; dS, rate of synonymous substitution.
This article has been cited by other articles:
|
|
 |
|
  P. J. Norman, L. Abi-Rached, K. Gendzekhadze, J. A. Hammond, A. K. Moesta, D. Sharma, T. Graef, K. L. McQueen, L. A. Guethlein, C. V.F. Carrington, et al. Meiotic recombination generates rich diversity in NK cell receptor genes, alleles, and haplotypes Genome Res., May 1, 2009; 19(5): 757 - 769. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. K. Moesta, L. Abi-Rached, P. J. Norman, and P. Parham Chimpanzees Use More Varied Receptors and Ligands Than Humans for Inhibitory Killer Cell Ig-Like Receptor Recognition of the MHC-C1 and MHC-C2 Epitopes J. Immunol., March 15, 2009; 182(6): 3628 - 3637. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. K. Moesta, P. J. Norman, M. Yawata, N. Yawata, M. Gleimer, and P. Parham Synergistic Polymorphism at Two Positions Distal to the Ligand-Binding Site Makes KIR2DL2 a Stronger Receptor for HLA-C Than KIR2DL3 J. Immunol., March 15, 2008; 180(6): 3969 - 3979. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
