Subfunctionalization of peroxisome proliferator response elements accounts for retention of duplicated fabp1 genes in zebrafish

Background: In the duplication-degeneration-complementation (DDC) model, a duplicated gene has three possible fates: it may lose functionality through the accumulation of mutations (non-functionalization), acquire a new function (neo-functionalization), or each duplicate gene may retain a subset of functions of the ancestral gene (sub-functionalization). The role that promoter evolution plays in retention of duplicated genes in eukaryotic genomes is not well understood. Fatty acid-binding proteins (Fabp) belong to a multigene family that are highly conserved in sequence and function, but differ in their gene regulation, suggesting selective pressure is exerted via regulatory elements in the promoter. A previous report showed that zebrafish fabp1b.1 and fabp1b.2 promoters underwent sub-functionalization of transcriptional control by peroxisome proliferator-activated receptors (PPAR). The fabp1b.1 promoter retained a functional PPAR response element (PPRE), while fabp1b.2 did not.
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