Evidence map›Paper›PMID 27421266›Full record

ArticleBMC evolutionary biology2016

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

Robert B Laprairie, Eileen M Denovan-Wright, Jonathan M Wright

Open access · goldAbstract read
In one paragraph

Article in BMC evolutionary biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  4. Comparing the effects of developmental exposure to alpha lipoic acid (ALA) and perfluorooctanesulfonic acid (PFOS) in zebrafish (Danio rerio).Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2024
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  13. Genome-Wide Analysis of theInternational journal of molecular sciences · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Robert B LaprairieDepartment of Pharmacology, Dalhousie University, 5850 College St, Halifax, NS, B3H 4R2, Canada.
Eileen M Denovan-WrightDepartment of Pharmacology, Dalhousie University, 5850 College St, Halifax, NS, B3H 4R2, Canada.
Jonathan M WrightDepartment of Biology, Dalhousie University, 31355 Oxford St, PO Box 15000, Halifax, NS, B3H 4R2, Canada. jmwright@dal.ca.
Dalhousie University · CA

Funding

CIHR
6 · The paper itself

Abstract

backgroundIn 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.

resultsIn 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.

conclusionsThe 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.

Indexed as

Gene DuplicationGenes, DuplicatePeroxisome ProliferatorsAnimalsFatty Acid-Binding ProteinsGene Expression RegulationHumansMutationPPAR alphaPromoter Regions, GeneticResponse ElementsZebrafishZebrafish ProteinsFatty Acid-Binding ProteinsPeroxisome ProliferatorsPPAR alphaZebrafish ProteinsDual luciferase assayFatty acid-binding proteinGene promoter evolutionNeofunctionalizationNonfunctionalizationPeroxisome proliferator activated receptor (PPAR)Spotted garSubfunctionalizationTeleost fishesZebrafish

Identifiers

PMID27421266
PMCPMC4947323
OpenAlexW2467977300

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.