Physical mapping and characterization of the equine lymphocyte antigen (ELA) complex
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Abstract
The major histocompatibility complex (MHC) is a genomic region comprised of a linked cluster of genes and gene families that play an important role in both the adaptive and innate immune responses. Genes within the MHC have also been associated with susceptibility and/or resistance to certain diseases, such as haemochromatosis, insulindependent diabetes, and psoriasis. As a result of these associations the MHC is one the most extensively studied regions of the mammalian genome. The MHCs of a wide variety of species, such as human (HLA), mouse (H-2), pig (SLA), and cow (BoLA), have been characterized with respect to gene content, genomic organization of class I, class II, and class III regions, and comparative organization. Comparative analyses have been useful in delineating the evolutionary development of the MHC. While the MHC of many mammalian species has been investigated, little research has been performed on the equine (Equus caballus) MHC. The equine MHC is referred to as the equine lymphocyte antigen (ELA) complex and is located on chromosome ECA20q. The research that has been done on ELA focused on identifying gene copy number and genetic polymorphisms in the classical class I and class II genes. To better characterize the gene content and organization of ELA, we isolated 103 bacterial artificial chromosome (BAC) clones from a horse BAC library containing well conserved genes found within mammalian MHCs. These BAC clones were assembled into two sequence-ready ordered contigs that span the ELA complex. The first contig which has a minimum tiling path of nine BAC clones contains the ELA class II region and spans 800 kb. The class I and III regions are contained within the second contig which has a 14 BAC clone minimum tiling path and spans 1.6 Mb. This study will report on the construction of the two BAC contigs which span the ELA complex, and characterization of the gene content and organization of the ELA complex.