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The Journal of Immunology, 2007, 178, 7162 -7172
Copyright © 2007 by The American Association of Immunologists, Inc.

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Extended Gene Map Reveals Tripartite Motif, C-Type Lectin, and Ig Superfamily Type Genes within a Subregion of the Chicken MHC-B Affecting Infectious Disease1,2

Takashi Shiina*, W. Elwood Briles{dagger}, Ronald M. Goto{ddagger}, Kazuyoshi Hosomichi*, Kazuyo Yanagiya*, Sayoko Shimizu*, Hidetoshi Inoko* and Marcia M. Miller3,{ddagger}

* Division of Basic Medical Science and Molecular Medicine, Department of Molecular Life Science, Tokai University School of Medicine, Kanagawa, Japan; {dagger} Department of Biological Sciences, Northern Illinois University, DeKalb, IL 60115; and {ddagger} Division of Molecular Biology, Beckman Research Institute, City of Hope National Medical Center, Duarte, CA 91010

MHC haplotypes have a remarkable influence on whether tumors form following infection of chickens with oncogenic Marek’s disease herpesvirus. Although resistance to tumor formation has been mapped to a subregion of the chicken MHC-B region, the gene or genes responsible have not been identified. A full gene map of the subregion has been lacking. We have expanded the MHC-B region gene map beyond the 92-kb core previously reported for another haplotype revealing the presence of 46 genes within 242 kb in the Red Jungle Fowl haplotype. Even though MHC-B is structured differently, many of the newly revealed genes are related to loci typical of the MHC in other species. Other MHC-B loci are homologs of genes found within MHC paralogous regions (regions thought to be derived from ancient duplications of a primordial immune defense complex where genes have undergone differential silencing over evolutionary time) on other chromosomes. Still others are similar to genes that define the NK complex in mammals. Many of the newly mapped genes display allelic variability and fall within the MHC-B subregion previously shown to affect the formation of Marek’s disease tumors and hence are candidates for genes conferring resistance.

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 Science Foundation MCB-9604589, National Cancer Institute R21 CA105426, National Research Initiative Grant Nos. 2004-35205-14203 and 2006-35205-16678 from the U.S. Department of Agriculture Cooperative State Research, Education, and Extension Service, and Kakenhi (Grant-in-Aid for Scientific Research) on Priority Areas "Comparative Genomics" from the Ministry of Education, Culture, Sports, Science and Technology of Japan. BAC filters were provided through the U.S. Department of Agricultural Cooperative State Research, Education, and Extension Service Multi-State Research Committee NRSP-8.

2 The sequence(s) presented in this article has been submitted to GenBank under accession number(s) AB268588.

3 Address correspondence and reprint requests to Dr. Marcia M. Miller, Beckman Research Institute, City of Hope National Medical Center, 1450 East Duarte Road, Duarte, CA 91010. E-mail address: mamiller{at}coh.org

4 Abbreviations used in this paper: IgSF, Ig superfamily; BTN, butyrophilin; MOG, myelin oligodendrocyte glycoprotein; TRIM, tripartite motif; RJF, Red Jungle Fowl; BAC, bacterial artificial chromosome; CDS, coding sequence; BLAST, basic local alignment search tool; EST, expressed sequence tag; LTR, long terminal repeat; SNP, single nucleotide polymorphism; WGS, Whole Genome Shotgun.




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