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

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Resumen

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 exerted via regulatory elements in the promoter. Results: In this study, we describe the PPAR regulation of zebrafish fabp1a, fabp1b.1, and fabp1b.2 promoters and compare them to the PPAR regulation of the spotted gar fabp1 promoter, representative of the ancestral fabp1 gene. Evolution of the fabp1 promoter was inferred by sequence analysis, and differential PPAR-agonist activation of fabp1 promoter activity in zebrafish liver and intestine explant cells, and in HEK293A cells transiently transfected with wild-type and mutated fabp1promoter-reporter gene constructs. The promoter activity of spotted gar fabp1, representative of the ancestral fabp1, was induced by both PPARα- and PPARγ-specific agonists, but displayed a biphasic response to PPARα activation. Zebrafish fabp1a was PPARα-selective, fabp1b.1 was PPARγ-selective, and fabp1b.2 was not regulated by PPAR. Conclusions: The zebrafish fabp1 promoters underwent two successive rounds of subfunctionalization with respect to PPAR regulation leading to retention of three zebrafish fabp1 genes with stimuli-specific regulation. Using a pharmacological approach, we demonstrated here the divergent regulation of the zebrafish fabp1a, fabp1b.1, and fabp1b.2 with regard to subfunctionalization of PPAR regulation following two rounds of gene duplication.

Idioma originalEnglish
Número de artículo147
PublicaciónBMC Evolutionary Biology
Volumen16
N.º1
DOI
EstadoPublished - jul. 16 2016

Nota bibliográfica

Funding Information:
This work was supported by an National Sciences and Engineering Research Council Canada (NSERC) Grant to JMW, and a Bridge Funding Grant from Dalhousie University to EMD-W. RBL is supported by studentships from the Canadian Institutes of Health Research (CIHR), the Huntington Society of Canada, Killam Trusts, and Nova Scotia Health Research Foundation. None of these funding bodies influenced the design of the study or the collection, analysis, or interpretation of data presented in the manuscript.

Publisher Copyright:
© 2016 The Author(s).

ASJC Scopus Subject Areas

  • Ecology, Evolution, Behavior and Systematics

PubMed: MeSH publication types

  • Journal Article

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