Plant & Animal Genomes XIII Conference

January 15-19, 2005
Town & Country Convention Center
San Diego, CA

Characterization Of Paralogous Regions Of The Atlantic Salmon (Salmo salar) Genome

Leslie Mitchell¹ , Krzysztof Lubieniecki¹ , Siemon Ng¹ , Glenn Cooper² , Ruth Phillips³ , Ben Koop² , William S. Davidson¹

¹  Department of Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC, Canada

²  Department of Biology, University of Victoria, Victoria, BC, Canada

³  Department of Biological Sciences, Washington State University, Vancouver, Washington, USA

Gene and genome duplications have played a major role in vertebrate evolution. Salmonids provide a useful resource for studying the consequences of these events as their common ancestor underwent a genome duplication between 25 and 120 million years ago. To understand how a genome reorganizes itself to cope with duplicated chromosomes and the importance of gene duplications for evolution and adaptation, the Genomics Research on Atlantic Salmon Project (GRASP) is characterizing large regions of the Atlantic salmon genome known to contain paralogous stretches of DNA. The metallothionein gene, a locus that has remained duplicated since the tetraploidization event, was used to screen a large insert (190kb) Atlantic salmon genomic BAC library. BAC clones from each locus were identified and FISH was used to verify that the clones corresponded to different chromosomes. A representative BAC from each locus was chosen for shotgun cloning. Sequence analysis reveals the presence of five genes shared between the loci, in addition to metallothionein. The overall gene order (deadeye, metallothionein, BBS2, Lin10, CBFB, GNAO) is conserved between the loci. Comparative genomic analysis between salmon, human, chicken, and zebrafish reveals the existence of extraordinary conservation of synteny among these six genes, although chromosomal rearrangements have led to gene order variation. As predicted by the classical model of gene duplication, one copy of the BBS2 gene pair has accumulated deleterious mutations and has become a pseudogene. It is unclear at this time whether the other duplicate genes have undergone neofunctionalization or subfunctionalization as predicted by the Duplication-Degeneration-Complementation model.