PUBLICATION
Divergent evolution of cis-acting peroxisome proliferator-activated receptor elements that differentially control the tandemly duplicated fatty acid-binding protein genes, fabp1b.1 and fabp1b.2, in zebrafish
- Authors
- Laprairie, R.B., Denovan-Wright, E.M., Wright, J.M.
- ID
- ZDB-PUB-160527-1
- Date
- 2016
- Source
- Genome 59(6): 403-12 (Journal)
- Registered Authors
- Wright, Jonathan M.
- Keywords
- duplication génique, duplication–degeneration–complementation, duplication–dégénérescence–complémentation, fatty acid-binding protein, gene duplication, peroxisome proliferator-activated receptor, promoter, promoteur, protéine de liaison aux acides gras, récepteur activés par les proliférateurs de peroxysomes
- MeSH Terms
-
- Animals
- Base Sequence
- Evolution, Molecular
- Fatty Acid-Binding Proteins/genetics*
- Gene Duplication
- Genes, Duplicate
- Genetic Variation
- HEK293 Cells
- Humans
- Mutation
- Peroxisome Proliferator-Activated Receptors/genetics*
- Promoter Regions, Genetic
- RNA, Messenger/genetics
- Transfection
- Zebrafish/genetics*
- Zebrafish Proteins/genetics*
- PubMed
- 27228313 Full text @ Genome
Citation
Laprairie, R.B., Denovan-Wright, E.M., Wright, J.M. (2016) Divergent evolution of cis-acting peroxisome proliferator-activated receptor elements that differentially control the tandemly duplicated fatty acid-binding protein genes, fabp1b.1 and fabp1b.2, in zebrafish. Genome. 59(6):403-12.
Abstract
Gene duplication is thought to facilitate increasing complexity in the evolution of life. The fate of most duplicated genes is nonfunctionalization: functional decay resulting from the accumulation of mutations. According to the duplication-degeneration-complementation (DDC) model, duplicated genes are retained by subfunctionalization, where the functions of the ancestral gene are sub-divided between duplicate genes, or by neofunctionalization, where one of the duplicates acquires a new function. Here, we report the differential regulation of the zebrafish tandemly duplicated fatty acid-binding protein genes, fabp1b.1 and fabp1b.2, by peroxisome proliferator-activated receptors (PPAR). fabp1b.1 mRNA levels were induced in tissue explants of liver, but not intestine, by PPAR agonists. fabp1b.1 promoter activity was induced to a greater extent by rosiglitazone (PPARγ-selective agonist) compared to WY 14,643 (PPARα-selective agonist) in HEK293A cells. Mutation of a peroxisome proliferator response element (PPRE) at -1232 bp in the fabp1b.1 promoter reduced PPAR-dependent activation. fabp1b.2 promoter activity was not affected by PPAR agonists. Differential regulation of the duplicated fabp1b promoters may be the result of PPRE loss in fabp1b.2 during a meiotic crossing-over event. Retention of PPAR inducibility in fabp1b.1 and not fabp1b.2 suggests unique regulation and function of the fabp1b duplicates.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping