Cited by 141melanin and skin pigmentationZebrafish Biomedical Research ApplicationsDevelopmental Biology and Gene Regulation

Pigment Pattern in jaguar/obelix Zebrafish Is Caused by a Kir7.1 Mutation: Implications for the Regulation of Melanosome Movement

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Iwashita, Motoko, Watanabe, Masakatsu, Ishii, Masaru, Chen, Tim, Johnson, Stephen L., Kurachi, Yoshihisa, Okada, Norihiro, Kondo, Shigeru·2006·PLoS Genetics

Abstract

Many animals have a variety of pigment patterns, even within a species, and these patterns may be one of the driving forces of speciation. Recent molecular genetic studies on zebrafish have revealed that interaction among pigment cells plays a key role in pattern formation, but the mechanism of pattern formation is unclear. The zebrafish jaguar/obelix mutant has broader stripes than wild-type fish. In this mutant, the development of pigment cells is normal but their distribution is altered, making these fish ideal for studying the process of pigment pattern formation. Here, we utilized a positional cloning method to determine that the inwardly rectifying potassium channel 7.1 (Kir7.1) gene is responsible for pigment cell distribution among jaguar/obelix mutant fish. Furthermore, in jaguar/obelix mutant alleles, we identified amino acid changes in the conserved region of Kir7.1, each of which affected K(+) channel activity as demonstrated by patch-clamp experiments. Injection of a bacterial artificial chromosome containing the wild-type Kir7.1 genomic sequence rescued the jaguar/obelix phenotype. From these results, we conclude that mutations in Kir7.1 are responsible for jaguar/obelix. We also determined that the ion channel function defect of melanophores expressing mutant Kir7.1 altered the cellular response to external signals. We discovered that mutant melanophores cannot respond correctly to the melanosome dispersion signal derived from the sympathetic neuron and that melanosome aggregation is constitutively activated. In zebrafish and medaka, it is well known that melanosome aggregation and subsequent melanophore death increase when fish are kept under constant light conditions. These observations indicate that melanophores of jaguar/obelix mutant fish have a defect in the signaling pathway downstream of the alpha2-adrenoceptor. Taken together, our results suggest that the cellular defect of the Kir7.1 mutation is directly responsible for the pattern change in the jaguar/obelix mutant.

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Crossref · 10.1371/journal.pgen.0020197

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  • kcnj13 encodes a potassium channel required in melanophores for interactions with xanthophores and iridophores, regulating the shapes of all three pigment cell types.

    “The kcnj13 gene encodes a potassium channel required in melanophores for interactions with xanthophores and iridophores, regulating the shapes of all three pigment cell types10–13.”

    From Genomic and genetic insights into speciation and pigment pattern diversification in <i>Danio</i> fishes (2025) · cites this paper as [11]

    The Results identify Kir7.1 as a potassium channel expressed in melanophores and xanthophores. The Discussion says it is thought to contribute to interactions between those cells, but does not establish that it is required for those interactions. The cited passages do not address interactions with iridophores or regulation of the shapes of all three pigment cell types. Page numbers are unavailable in our copy. (LLM, conf=0.88)

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Authors
Iwashita, M., Watanabe, M., Ishii, M., Chen, T., Johnson, S. L., Kurachi, Y., Okada, N., & Kondo, S.
Affiliations
  • Tokyo Institute of Technology (JP)
  • The University of Osaka (JP)
  • Washington University in St. Louis (US)
  • RIKEN (JP)
Corresponding author
Kondo, Shigeru
Venue
PLoS Genetics
Published
2006
Volume
2
Issue
11
Pages
e197
ISSN
  • 1553-7390 (ISSN-L)
  • 1553-7404
OpenAlex
W1979736337
Cited by
141
References
0
Citations by year
2026: 6 · 2025: 4 · 2024: 3 · 2023: 6 · 2021: 10 · 2020: 10 · 2019: 9 · 2018: 11 · 2017: 15 · 2016: 6 · 2015: 7 · 2014: 11 · 2013: 6 · 2012: 12
FWCI
2.18
Type
journal article
Language
en
Open access
Locations
  • PLoS Genetics (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
  • Figshare (submittedVersion, cc-by)
  • Institutional Repositories DataBase (IRDB) (submittedVersion)
  • Tokyo Tech Research Repository (Tokyo Institute of Technology) (submittedVersion)
Funders
  • Ministry of Education, Culture, Sports, Science and Technology
  • National Institutes of Health
  • Japan Society for the Promotion of Science (12144207)
  • National Institute of General Medical Sciences (GM56988, R01GM056988, R56GM056988)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Zebrafish Biomedical Research Applications
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
Keywords
zebrafish, Kir7.1, inwardly rectifying potassium channels, pigment pattern formation, melanophores, melanosome dispersion, positional cloning, speciation
MeSH terms
Adrenergic Agonists, Amino Acid Sequence, Animals, Biological Transport, Cloning, Molecular, Gene Expression Regulation, Humans, Melanophores, Molecular Sequence Data, Mutation, Phenotype, Pigmentation, RNA, Messenger, Zebrafish, Signal Transduction, Sequence Alignment, Protein Structure, Secondary, Receptors, Adrenergic, alpha-2, Adrenergic Antagonists, Melanosomes, Potassium Channels, Inwardly Rectifying, Adrenergic alpha-2 Receptor Agonists, Adrenergic alpha-2 Receptor Antagonists

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