Differential regulation of the duplicated fatty acid-binding protein genes in teleost fishes

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In 1970, Susumu Ohno proposed the major mechanism that facilitates increasing complexity in the evolution of life is gene duplication. Allan Force and others revisited this idea in the Duplication-Degeneration-Complementation (DDC) model in which duplicated genes are retained in the genome either by subfunctionalization, where the functions of the ancestral gene are sub-divided between the sister duplicate genes, or by neofunctionalization, where one of the duplicates acquires a new function. In this model, both processes for retention of duplicated genes occur by either loss or gain of regulatory elements in the promoters of sister duplicate genes. The common fate of a duplicated gene, however, is nonfunctionalization, the accumulation of deleterious mutations resulting in functional decay. The long-term goal of this research program is to test the hypothesis of the DDC model that duplicated genes are retained in the genome by either sub- or neofunctionalization. The work proposed in this Discovery Grant proposal focusses on the regulation of the duplicated copies of the multigene family of the intracellular lipid-binding protein (iLBP) genes that code for the fatty acid- (