Journal of Heredity Advance Access published online on August 3, 2007
Journal of Heredity, doi:10.1093/jhered/esm056
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Comparative Genomic Structure of Human, Dog, and Cat MHC: HLA, DLA, and FLA
From the Laboratory of Genomic Diversity, National Cancer Institute at Frederick, Frederick, MD 21702-1201 (Yuhki, O'Brien); SAIC-Frederick, National Cancer Institute at Frederick, Frederick, MD 21702-1201 (Beck); the Advanced Biomedical Computing Center, National Cancer Institute at Frederick, Frederick, MD 21702-1201 (Stephens, Neelam)
Address correspondence to Dr. Naoya Yuhki at the address above, or e-mail: yuhki{at}ncifcrf.gov.
Comparisons of the genomic structure of 3 mammalian major histocompatibility complexes (MHCs), human HLA, canine DLA, and feline FLA revealed remarkable structural differences between HLA and the other 2 MHCs. The 4.6-Mb HLA sequence was compared with the 3.9-Mb DLA sequence from 2 supercontigs generated by 7x whole-genome shotgun assembly and 3.3-Mb FLA draft sequence. For FLA, we confirm that 1) feline FLA was split into 2 pieces within the TRIM (member of the tripartite motif) gene family found in human HLA, 2) class II, III, and I regions were placed in the pericentromeric region of the long arm of chromosome B2, and 3) the remaining FLA was located in subtelomeric region of the short arm of chromosome B2. The exact same chromosome break was found in canine DLA structure, where class II, III, and I regions were placed in a pericentromeric region of chromosome 12 whereas the remaining region was located in a subtelomeric region of chromosome 35, suggesting that this chromosome break occurred once before the split of felid and canid more than 55 million years ago. However, significant differences were found in the content of genes in both pericentromeric and subtelomeric regions in DLA and FLA, the gene number, and amplicon structure of class I genes plus 2 other class I genes found on 2 additional chromosomes; canine chromosomes 7 and 18 suggest the dynamic nature in the evolution of MHC class I genes.
This work was presented in poster form at the Third International Conference on Advances in Canine and Feline Genomics and Inherited Diseases, Davis, CA, August 2006.