Subfunctionalization of peroxisome proliferator response elements accounts for retention of duplicated fabp1 genes in zebrafish. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Laprairie, Robert; Denovan-Wright, Eileen; Wright, Jonathan
• Is Part Of: BMC evolutionary biology. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 15
• Publication Date: 2016-12
• Subjects: Peroxisome proliferator activated receptor (PPAR) -- Dual luciferase assay -- Fatty acid-binding protein -- Subfunctionalization -- Neofunctionalization -- Nonfunctionalization -- Teleost fishes -- Gene promoter evolution -- Zebrafish -- Spotted gar; Evolution (Biology) -- Periodicals; 576.805
• DOI: 10.1186/s12862-016-0717-x
• Languages: English
• ISSNs: 1471-2148

Abstract

Abstract Background In the duplication-degeneration-complementation (DDC) model, a duplicated gene has three possible fates: it may lose functionality through the accumulation of mutations (nonfunctionalization), acquire a new function (neofunctionalization), or each duplicate gene may retain a subset of functions of the ancestral gene (subfunctionalization). 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 exertedvia regulatory elements in the promoter. Results In this study, we describe the PPAR regulation of zebrafishfabp1a, fabp1b.1, andfabp1b.2 promoters and compare them to the PPAR regulation of the spotted garfabp1 promoter, representative of the ancestralfabp1 gene. Evolution of thefabp1 promoter was inferred by sequence analysis, and differential PPAR-agonist activation offabp1 promoter activity in zebrafish liver and intestine explant cells, and in HEK293A cells transiently transfected with wild-type and mutatedfabp1 promoter-reporter gene constructs. The promoter activity of spotted garfabp1, representative of the ancestralfabp1, was induced by both PPARα- and PPARγ-specific agonists, but displayed a biphasic response to PPARα activation. Zebrafishfabp1a was PPARα-selective, fabp1b.1 was PPARγ-selective, andfabp1b.2 was not regulated by PPAR. Conclusions The zebrafishfabp1 promoters underwent two successive rounds of subfunctionalization with respect to PPAR regulation leading to retention of three zebrafishfabp1 genes with stimuli-specific regulation. Using a pharmacological approach, we demonstrated here the divergent regulation of the zebrafishfabp1a, fabp1b.1, andfabp1b.2 with regard to subfunctionalization of PPAR regulation following two rounds of gene duplication.