Evidence map›Paper›PMID 31929524›Full record

ArticlePLoS genetics2020

Dysfunction of Oskyddad causes Harlequin-type ichthyosis-like defects in Drosophila melanogaster.

Yiwen Wang, Michaela Norum, Kathrin Oehl, Yang Yang, Renata Zuber, Jing Yang, Jean-Pierre Farine, Nicole Gehring, Matthias Flötenmeyer, Jean-François Ferveur and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 42 citations in OpenAlex.

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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

11 authors at 5 institutions in 3 countries.

Yiwen WangSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.ORCID 0000-0003-2069-6685
Michaela NorumSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.ORCID 0000-0002-5669-4801
Kathrin OehlSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.
Yang YangSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.
Renata ZuberSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.
Jing YangSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.
Jean-Pierre FarineCentre des Sciences du Goût et de l'Alimentation, UMR-CNRS 6265, Université de Bourgogne, Dijon, France.
Nicole GehringSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.
Matthias FlötenmeyerMicroscopy Unit, Max-Planck-Institut für Entwicklungsbiologie, Tübingen, Germany.
Jean-François FerveurCentre des Sciences du Goût et de l'Alimentation, UMR-CNRS 6265, Université de Bourgogne, Dijon, France.ORCID 0000-0002-4022-686X
Bernard MoussianSection Animal Genetics, Interfaculty Institute of Cell Biology, University of Tübingen, Tübingen, Germany.ORCID 0000-0002-2854-9500
University of Tübingen · DECentre National de la Recherche Scientifique · FRMax Planck Society · DETechnische Universität Dresden · DETianjin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prevention of desiccation is a constant challenge for terrestrial organisms. Land insects have an extracellular coat, the cuticle, that plays a major role in protection against exaggerated water loss. Here, we report that the ABC transporter Oskyddad (Osy)-a human ABCA12 paralog-contributes to the waterproof barrier function of the cuticle in the fruit fly Drosophila melanogaster. We show that the reduction or elimination of Osy function provokes rapid desiccation. Osy is also involved in defining the inward barrier against xenobiotics penetration. Consistently, the amounts of cuticular hydrocarbons that are involved in cuticle impermeability decrease markedly when Osy activity is reduced. GFP-tagged Osy localises to membrane nano-protrusions within the cuticle, likely pore canals. This suggests that Osy is mediating the transport of cuticular hydrocarbons (CHC) through the pore canals to the cuticle surface. The envelope, which is the outermost cuticle layer constituting the main barrier, is unaffected in osy mutant larvae. This contrasts with the function of Snu, another ABC transporter needed for the construction of the cuticular inward and outward barriers, that nevertheless is implicated in CHC deposition. Hence, Osy and Snu have overlapping and independent roles to establish cuticular resistance against transpiration and xenobiotic penetration. The osy deficient phenotype parallels the phenotype of Harlequin ichthyosis caused by mutations in the human abca12 gene. Thus, it seems that the cellular and molecular mechanisms of lipid barrier assembly in the skin are conserved during evolution.

Indexed as

ATP-Binding Cassette TransportersDesiccationDrosophila ProteinsIchthyosis, LamellarLoss of Function MutationATP-Binding Cassette TransportersDrosophila Proteinsosy protein, Drosophilasnu protein, Drosophila

Identifiers

PMID31929524
PMCPMC6980720
OpenAlexW2999447462

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.