Interplay between Foxd3 and Mitf regulates cell fate plasticity in the zebrafish neural crest
Open accessAbstract
Pigment cells of the zebrafish, Danio rerio, offer an exceptionally tractable system for studying the genetic and cellular bases of cell fate decisions. In the zebrafish, neural crest cells generate three types of pigment cells during embryogenesis: yellow xanthophores, iridescent iridophores and black melanophores. In this study, we present evidence for a model whereby melanophores and iridophores descend from a common precursor whose fate is regulated by an interplay between the transcription factors Mitf and Foxd3. Loss of mitfa, a key regulator of melanophore development, resulted in supernumerary ectopic iridophores while loss of foxd3, a mitfa repressor, resulted in fewer iridophores. Double mutants showed a restoration of iridophores, suggesting that one of Foxd3's roles is to suppress mitfa to promote iridophore development. Foxd3 co-localized with pnp4a, a novel marker of early iridophore development, and was necessary for its expression. A considerable overlap was found between iridoblast and melanoblast markers but not xanthoblast markers, which resolved as cells began to differentiate. Cell lineage analyses using the photoconvertible marker, EosFP, revealed that both melanophores and iridophores develop from a mitfa+ precursor. Taken together, our data reveal a Foxd3/mitfa transcriptional switch that governs whether a bi-potent pigment precursor will attain either an iridophore or a melanophore fate.
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Many genes previously known to be expressed by iridophores are components of the purine synthesis pathway.
“Many of the genes previously known to be expressed by iridophores are components of the purine synthesis pathway, as iridophore pigment largely consists of stacks of guanine plates [30], [71].”
From Gene Expression Analysis of Zebrafish Melanocytes, Iridophores, and Retinal Pigmented Epithelium Reveals Indicators of Biological Function and Developmental Origin (2013) · cites this paper as [71]
The Results section (‘pnp4a is a novel iridoblast marker’; page not provided) identifies pnp4a as an iridophore marker. The Discussion (‘pnp4a as a novel iridophore marker’; page not provided) links its enzyme family to purine synthesis and iridescence to guanine crystals. This supports one example, but not the claim that many known iridophore-expressed genes are purine-synthesis components. (LLM, conf=0.86)
Experimental — accuracy not yet measuredFoxd3 maintains pluripotency of neural crest cells and later contributes to specifying neuronal, glial, and iridophore fates over melanocyte or melanophore fates.
“Foxd3 maintains pluripotency of neural crest cells and later contributes to specifying neuronal, glial, and iridophore fates over melanocyte or melanophore fates (51, 52, 60) and is regulated by BMP signals in other contexts (61, 62).”
From Agouti and BMP signaling drive a naturally occurring fate conversion of melanophores to leucophores in zebrafish (2025) · cites this paper as [52]
The Introduction (page unavailable) reports evidence that Foxd3 promotes iridophore development and blocks melanophore development. The Results section, “Foxd3 is necessary for pnp4a expression” (page unavailable), notes Foxd3 expression in glia and neurons, but does not establish that it specifies those fates. The paper describes neural crest cells as multipotent; it does not show that Foxd3 maintains their pluripotency. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIridophore pigment largely consists of stacks of guanine plates.
“Many of the genes previously known to be expressed by iridophores are components of the purine synthesis pathway, as iridophore pigment largely consists of stacks of guanine plates [30], [71].”
In homozygous tfec mutants, expression of pnp4a was largely undetectable at 48 hpf.
“In homozygous tfec mutants, expression of the differentiated iridophore marker, pnp4a [14, 17], was largely undetectable at 48 hpf (Figs 5E and 5F and S3), consistent with complete lack of differentiated iridophores in tfec mutants.”
From The MITF paralog tfec is required in neural crest development for fate specification of the iridophore lineage from a multipotent pigment cell progenitor (2021) · cites this paper as [17]
Mitfa is excluded as a potential Tfec cofactor, as it is not essential for iridophore specification.
“The immediate MiT family candidate, Mitfa, is excluded as a potential Tfec cofactor, as it is not essential for iridophore specification [17].”
From The MITF paralog tfec is required in neural crest development for fate specification of the iridophore lineage from a multipotent pigment cell progenitor (2021) · cites this paper as [17]
Marker analyses and lineage-tracing experiments support the existence of a bipotent melanocyte-iridophore (MI) precursor, the fate of which is influenced by foxd3/mitfa interaction.
“In the absence of foxd3, iridophore numbers are reduced in a manner that is at least partially mitfa-dependent, and marker analyses and lineage-tracing experiments support the existence of a bipotent melanocyte-iridophore (MI) precursor, the fate of which is influenced by this foxd3/mitfa interaction [12, 17].”
From The MITF paralog tfec is required in neural crest development for fate specification of the iridophore lineage from a multipotent pigment cell progenitor (2021) · cites this paper as [17]
In the absence of foxd3, iridophore numbers are reduced in a manner that is at least partially mitfa-dependent.
“In the absence of foxd3, iridophore numbers are reduced in a manner that is at least partially mitfa-dependent, and marker analyses and lineage-tracing experiments support the existence of a bipotent melanocyte-iridophore (MI) precursor, the fate of which is influenced by this foxd3/mitfa interaction [12, 17].”
From The MITF paralog tfec is required in neural crest development for fate specification of the iridophore lineage from a multipotent pigment cell progenitor (2021) · cites this paper as [17]
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- Authors
- Curran, K., Lister, J. A., Kunkel, G. R., Prendergast, A., Parichy, D. M., & Raible, D. W.
- Affiliations
- University of Washington (US)
- Virginia Commonwealth University (US)
- Texas A&M University (US)
- Corresponding author
- Raible, David W.
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2010-08
- Volume
- 344
- Issue
- 1
- Pages
- 107-118
- ISSN
- 0012-1606 (ISSN-L)
- PMC
- PMC2909359
- OpenAlex
- W2040365962
- Cited by
- 170
- References
- 0
- Citations by year
- 2026: 12 · 2025: 9 · 2024: 7 · 2023: 7 · 2022: 8 · 2021: 18 · 2020: 9 · 2019: 6 · 2018: 12 · 2017: 14 · 2016: 8 · 2015: 9 · 2014: 13 · 2013: 14 · 2012: 16
- FWCI
- 4.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS057220, R01NS045246)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32HD007183)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › melanin and skin pigmentation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Zebrafish Biomedical Research Applications
- Keywords
- FOXD3, MITF, mitfa, neural crest, pigment cells, iridophores, melanophores, xanthophores, cell fate plasticity, transcriptional switch, lineage tracing, zebrafish embryonic development
- MeSH terms
- Animals, Melanocytes, Microscopy, Fluorescence, Models, Biological, Models, Genetic, Mutation, Neural Crest, Phylogeny, Pigmentation, Zebrafish, Gene Expression Regulation, Developmental, Cell Lineage, Zebrafish Proteins, Animals, Genetically Modified, Microphthalmia-Associated Transcription Factor, Forkhead Transcription Factors
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