Evidence map›Paper›PMID 28103795›Full record

ArticleBMC evolutionary biology2017

Lineage-specific duplication of amphioxus retinoic acid degrading enzymes (CYP26) resulted in sub-functionalization of patterning and homeostatic roles.

João E Carvalho, Maria Theodosiou, Jie Chen, Pascale Chevret, Susana Alvarez, Angel R De Lera, Vincent Laudet, Jenifer C Croce, Michael Schubert

Open access · goldAbstract read
In one paragraph

Article in BMC evolutionary biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
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  4. A Functional Polymorphism Downstream of Vitamin A Regulator GeneInternational journal of molecular sciences · 2023
    Article
  5. Review
  6. Article
  7. Article
  8. New luciferin-based probe substrates for human CYP26A1.Biochemistry and biophysics reports · 2020
    Article
  9. Article
  10. Review
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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

9 authors at 3 institutions in 3 countries.

João E CarvalhoSorbonne Universités, UPMC Université Paris 06, CNRS, Laboratoire de Biologie du Développement de Villefranche-sur-Mer, Observatoire Océanologique de Villefranche-sur-Mer, 181 Chemin du Lazaret, 06230, Villefranche-sur-Mer, France.
Maria TheodosiouMolecular Zoology Team, Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Université Lyon 1, CNRS, INRA, Ecole Normale Supérieure de Lyon, 46 Allée d'Italie, 69364, Lyon, Cedex 07, France.
Jie ChenMolecular Zoology Team, Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Université Lyon 1, CNRS, INRA, Ecole Normale Supérieure de Lyon, 46 Allée d'Italie, 69364, Lyon, Cedex 07, France.
Pascale ChevretLaboratoire de Biométrie et Biologie Evolutive, Université de Lyon, Université Lyon 1, CNRS, 43 Boulevard du 11 novembre 1918, 69622, Villeurbanne, France.
Susana AlvarezDepartamento de Química Organica, Facultad de Química, Universidade de Vigo, 36310, Vigo, Spain.
Angel R De LeraDepartamento de Química Organica, Facultad de Química, Universidade de Vigo, 36310, Vigo, Spain.
Vincent LaudetMolecular Zoology Team, Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Université Lyon 1, CNRS, INRA, Ecole Normale Supérieure de Lyon, 46 Allée d'Italie, 69364, Lyon, Cedex 07, France.
Jenifer C CroceSorbonne Universités, UPMC Université Paris 06, CNRS, Laboratoire de Biologie du Développement de Villefranche-sur-Mer, Observatoire Océanologique de Villefranche-sur-Mer, 181 Chemin du Lazaret, 06230, Villefranche-sur-Mer, France.
Michael SchubertSorbonne Universités, UPMC Université Paris 06, CNRS, Laboratoire de Biologie du Développement de Villefranche-sur-Mer, Observatoire Océanologique de Villefranche-sur-Mer, 181 Chemin du Lazaret, 06230, Villefranche-sur-Mer, France. Michael.Schubert@obs-vlfr.fr.ORCID 0000-0002-2341-712X
Université Claude Bernard Lyon 1 · FRCentre National de la Recherche Scientifique · FRUniversidade de Vigo · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDuring embryogenesis, tight regulation of retinoic acid (RA) availability is fundamental for normal development. In parallel to RA synthesis, a negative feedback loop controlled by RA catabolizing enzymes of the cytochrome P450 subfamily 26 (CYP26) is crucial. In vertebrates, the functions of the three CYP26 enzymes (CYP26A1, CYP26B1, and CYP26C1) have been well characterized. By contrast, outside vertebrates, little is known about CYP26 complements and their biological roles. In an effort to characterize the evolutionary diversification of RA catabolism, we studied the CYP26 genes of the cephalochordate amphioxus (Branchiostoma lanceolatum), a basal chordate with a vertebrate-like genome that has not undergone the massive, large-scale duplications of vertebrates.

resultsIn the present study, we found that amphioxus also possess three CYP26 genes (CYP26-1, CYP26-2, and CYP26-3) that are clustered in the genome and originated by lineage-specific duplication. The amphioxus CYP26 cluster thus represents a useful model to assess adaptive evolutionary changes of the RA signaling system following gene duplication. The characterization of amphioxus CYP26 expression, function, and regulation by RA signaling demonstrated that, despite the independent origins of CYP26 duplicates in amphioxus and vertebrates, they convergently assume two main roles during development: RA-dependent patterning and protection against fluctuations of RA levels. Our analysis suggested that in amphioxus RA-dependent patterning is sustained by CYP26-2, while RA homeostasis is mediated by CYP26-1 and CYP26-3. Furthermore, comparisons of the regulatory regions of CYP26 genes of different bilaterian animals indicated that a CYP26-driven negative feedback system was present in the last common ancestor of deuterostomes, but not in that of bilaterians.

conclusionsAltogether, this work reveals the evolutionary origins of the RA-dependent regulation of CYP26 genes and highlights convergent functions for CYP26 enzymes that originated by independent duplication events, hence establishing a novel selective mechanism for the genomic retention of gene duplicates.

Indexed as

AnimalsCytochrome P450 Family 26Embryonic DevelopmentEvolution, MolecularGene DuplicationGenomeLanceletsSignal TransductionTretinoinCytochrome P450 Family 26TretinoinBranchiostoma lanceolatumCephalochordateDuplication-Degeneration-Complementation (DDC) modelLanceletRetinoic acid (RA) signaling

Identifiers

PMID28103795
PMCPMC5247814
OpenAlexW2571876439

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.