Evidence map›Paper›PMID 29621239›Full record

ArticlePLoS genetics2018

Distinct interactions of Sox5 and Sox10 in fate specification of pigment cells in medaka and zebrafish.

Yusuke Nagao, Hiroyuki Takada, Motohiro Miyadai, Tomoko Adachi, Ryoko Seki, Yasuhiro Kamei, Ikuyo Hara, Yoshihito Taniguchi, Kiyoshi Naruse, Masahiko Hibi and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 75 citations in OpenAlex.

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  9. Specialized molecular pathways drive the formation of light-scattering assemblies in leucophores.Proceedings of the National Academy of Sciences of the United States of America · 2025
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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

12 authors at 4 institutions in 2 countries.

Yusuke NagaoBioscience and Biotechnology Center and Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, Japan.
Hiroyuki TakadaBioscience and Biotechnology Center and Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, Japan.
Motohiro MiyadaiBioscience and Biotechnology Center and Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, Japan.
Tomoko AdachiBioscience and Biotechnology Center and Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, Japan.
Ryoko SekiBioscience and Biotechnology Center and Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, Japan.ORCID 0000-0003-4173-2067
Yasuhiro KameiDepartment of Basic Biology, School of Life Science, Graduate University of Advanced Studies (SOKENDAI), Myodaiji, Okazaki, Aichi, Japan.
Ikuyo HaraDepartment of Basic Biology, School of Life Science, Graduate University of Advanced Studies (SOKENDAI), Myodaiji, Okazaki, Aichi, Japan.
Yoshihito TaniguchiDepartment of Public Health and Preventive Medicine, Kyorin University, School of Medicine, Mitaka, Tokyo, Japan.ORCID 0000-0003-1141-5589
Kiyoshi NaruseDepartment of Basic Biology, School of Life Science, Graduate University of Advanced Studies (SOKENDAI), Myodaiji, Okazaki, Aichi, Japan.
Masahiko HibiBioscience and Biotechnology Center and Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, Japan.
Robert N KelshDepartment of Biology and Biochemistry, University of Bath, Claverton Down, Bath, United Kingdom.ORCID 0000-0002-9381-0066
Hisashi HashimotoBioscience and Biotechnology Center and Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho, Chikusa-ku, Nagoya, Aichi, Japan.ORCID 0000-0003-0089-9717
Nagoya University · JPNational Institute for Basic Biology · JPUniversity of Bath · GBKyorin University · JP

Funding

Medical Research Council MR/J001457/1
6 · The paper itself

Abstract

Mechanisms generating diverse cell types from multipotent progenitors are fundamental for normal development. Pigment cells are derived from multipotent neural crest cells and their diversity in teleosts provides an excellent model for studying mechanisms controlling fate specification of distinct cell types. Zebrafish have three types of pigment cells (melanocytes, iridophores and xanthophores) while medaka have four (three shared with zebrafish, plus leucophores), raising questions about how conserved mechanisms of fate specification of each pigment cell type are in these fish. We have previously shown that the Sry-related transcription factor Sox10 is crucial for fate specification of pigment cells in zebrafish, and that Sox5 promotes xanthophores and represses leucophores in a shared xanthophore/leucophore progenitor in medaka. Employing TILLING, TALEN and CRISPR/Cas9 technologies, we generated medaka and zebrafish sox5 and sox10 mutants and conducted comparative analyses of their compound mutant phenotypes. We show that specification of all pigment cells, except leucophores, is dependent on Sox10. Loss of Sox5 in Sox10-defective fish partially rescued the formation of all pigment cells in zebrafish, and melanocytes and iridophores in medaka, suggesting that Sox5 represses Sox10-dependent formation of these pigment cells, similar to their interaction in mammalian melanocyte specification. In contrast, in medaka, loss of Sox10 acts cooperatively with Sox5, enhancing both xanthophore reduction and leucophore increase in sox5 mutants. Misexpression of Sox5 in the xanthophore/leucophore progenitors increased xanthophores and reduced leucophores in medaka. Thus, the mode of Sox5 function in xanthophore specification differs between medaka (promoting) and zebrafish (repressing), which is also the case in adult fish. Our findings reveal surprising diversity in even the mode of the interactions between Sox5 and Sox10 governing specification of pigment cell types in medaka and zebrafish, and suggest that this is related to the evolution of a fourth pigment cell type.

Indexed as

Cell LineageAllelesAnimalsGene Expression Regulation, DevelopmentalMelanocytesNeural CrestOryziasPigmentationSOXD Transcription FactorsSOXE Transcription FactorsZebrafishZebrafish Proteinssox10 protein, zebrafishSox5 protein, zebrafishSOXD Transcription FactorsSOXE Transcription FactorsZebrafish Proteins

Identifiers

PMID29621239
PMCPMC5886393
OpenAlexW2796383848

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.