Pigment Cell Development in Teleosts

Hashimoto, Hisashi; Goda, Makoto; Kelsh, Robert N.

doi:10.1007/978-981-16-1490-3_7

Cited by 10 publications

(9 citation statements)

References 109 publications

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“…Mammals only have a single pigment cell-type (melanocyte), but most vertebrates (including zebrafish and medaka) have two or more pigment cell-types (collectively known as chromatophores), including melanocytes (black), xanthophores (yellow), iridophores (iridescent, usually blue or silver), leucophores (white or cream) and others (Fujii, 1993;Schartl et al, 2016). The genetic accessibility of these cells has ensured that pigment cells are a well-studied 'model-within-a-model' for NC development: for a recent review of the key concepts, see Hashimoto et al (Hashimoto et al, 2021). Here, we will confine our attention to the proposed cell intermediates within pigment cell development in fish, which together formulate a widely-accepted PFR model of pigment cell development.…”

Section: The Chromatoblast and Bipotent Pigment Cell Progenitorsmentioning

confidence: 99%

Cyclical fate restriction: a new view of neural crest cell fate specification

et al. 2021

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Neural crest cells are crucial in development, not least because of their remarkable multipotency. Early findings stimulated two hypotheses for how fate specification and commitment from fully multipotent neural crest cells might occur, progressive fate restriction (PFR) and direct fate restriction, differing in whether partially restricted intermediates were involved. Initially hotly debated, they remain unreconciled, although PFR has become favoured. However, testing of a PFR hypothesis of zebrafish pigment cell development refutes this view. We propose a novel ‘cyclical fate restriction’ hypothesis, based upon a more dynamic view of transcriptional states, reconciling the experimental evidence underpinning the traditional hypotheses.

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Section: The Chromatoblast and Bipotent Pigment Cell Progenitorsmentioning

confidence: 99%

Cyclical fate restriction: a new view of neural crest cell fate specification

et al. 2021

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“…For instance, the tyrosinase mutant displays melanophore defects, similar to our albino phenotype ( Koga et al 1995 ), while the oca2 mutant has milder melanophore formation defects ( Fukamachi et al 2004 ). Although many studies have investigated melanophores in medaka ( Hashimoto et al 2021 ), this is the first to report that hps1 mutation causes an albino phenotype in medaka. The findings also demonstrate that the survival rate of albino fish was comparable to that of their black siblings; however, the shorter body length of albino fish suggests low competitiveness in getting food even in the laboratory environment ( Fig.…”

Section: Discussionmentioning

confidence: 89%

Evolutionarily conserved role of hps1 in melanin production and blood coagulation in medaka fish

Iwanami

Ozaki

Sakaguchi

et al. 2022

G3 Genes|Genomes|Genetics

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Hermansky-Pudlak syndrome is an autosomal recessive disease characterized by albinism, visual impairment, and blood platelet dysfunction. One of the genes responsible for Hermansky-Pudlak syndrome, hps1, regulates organelle biogenesis and thus plays important roles in melanin production, blood clotting, and the other organelle-related functions in humans and mice. However, the function of hps1 in other species remains poorly understood. In this study, we discovered albino medaka fish during the maintenance of a wild-derived population and identified hps1 as the responsible gene using positional cloning. In addition to the specific absence of melanophore pigmentation, the hps1 mutant showed reduced blood coagulation, suggesting that hps1 is involved in clotting caused by both mammalian platelets and fish thrombocytes. Together, the findings of our study demonstrate that hps1 has an evolutionarily conserved role in melanin production and blood coagulation. In addition, our study presents a useful vertebrate model for understanding the molecular mechanisms of Hermansky-Pudlak syndrome.

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“…This may suggest that the role of the eda / edar / edaradd pathway is not directly involved in the fin epidermal development but upstream. In addition, the pigment cells (fluoroleucophore, Hashimoto et al , 2021) are accumulated at the tip of the tail inside of the caudal fin fold suggesting that neural crest cell differentiation to pigment cells in the caudal fin was not suppressed either. Considering this evidence, although all cell linage are missing in the caudal fin ray, it is possible that the role of this pathway is highly specific to a cell lineage such as cartilage cell differentiation as previously suggested and defects in other cell lineage may be a secondary consequence of the defect (Iida et al ., 2014; Sadier et al ., 2014; Lefebvre and Mikkola, 2014).…”

Section: Discussionmentioning

confidence: 99%

Developmental defects in ectodermal appendages caused by missense mutation inedaraddgene in thenfrmangrove killifish,Kryptolebias marmoratus

Saud,

O’Neill,

Ring

et al. 2024

Preprint

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From an ENU-mutated mangrove killifish line R228, we have identified and isolated a novel mutant line, no-fin-ray/nfr in which fin ray development is largely reduced. Besides the reduction of the fin, the nfr mutant also exhibited other phenotype associated with ectodermal cell lineages including loss of scales, deformation in the gill structure such as decreasing the number of gill filaments, the reduction in the number of jaw teeth, pharyngeal teeth and gill rakers. Illumina RNAseq with 12 embryos each from mutants, siblings and the parental WT strain Hon9 identified a mutation in the edaradd in a highly conserved C-terminal death domain. Edaradd is known as a cytoplasmic accessory protein for the Ectodysplasin A (EDA) signalling pathway. To confirm the crucial role of edaradd during fin development, CRISPR RNAs were designed to knock out the gene in another killifish species, Arabian killifish. Indeed, Arabian killifish edaradd crispants showed a potent reduction of the fin development with 100% frequency. Furthermore, EDA crispants also showed identical phenotypes to that of edaradd crispants, confirming the fin defect in the mutants/crispants is caused by the signalling pathway of the EDA in the killifish species. These data demonstrate a powerful genetic approach using isogenic self-fertilising mangrove killifish as a tool for identifying mutants and their mutation, and revealed the crucial role of edaradd in the fish fin development and other ectoderm derived epithelial tissues.

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Pigment Cell Development in Teleosts

Cited by 10 publications

References 109 publications

Cyclical fate restriction: a new view of neural crest cell fate specification

Cyclical fate restriction: a new view of neural crest cell fate specification

Evolutionarily conserved role of hps1 in melanin production and blood coagulation in medaka fish

Developmental defects in ectodermal appendages caused by missense mutation inedaraddgene in thenfrmangrove killifish,Kryptolebias marmoratus

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