The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The requested protein is correctly identified. Q9PWC2 corresponds to zebrafish (Danio rerio) Mitfa, historically encoded by the nacre locus, and is distinct from the teleost paralog mitfb. The literature consistently describes Mitfa as a MiT/TFE-family basic helix–loop–helix leucine-zipper transcription factor required for neural-crest-derived melanophore development, matching the supplied protein description and bHLH, MiT/TFE-N and MiT/TFE-C annotations. No conflicting use of mitfa for a different protein was encountered. (steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8, miyadai2023ageneregulatory pages 1-2)
Its primary molecular function is sequence-specific transcriptional regulation, not enzymatic catalysis or transport. Mitfa acts in the nucleus to establish and maintain pigment-cell gene-expression programs. The strongest zebrafish evidence places it at the core of melanophore specification and differentiation, with additional context-dependent functions in xanthophore development and adult melanocyte regeneration. In contrast, Mitfa is not individually or jointly with Mitfb essential for zebrafish retinal pigment epithelium development. (miyadai2023ageneregulatory pages 1-2, lane2012otxbutnot pages 1-2)
| Annotation aspect | Best-supported conclusion | Evidence type / strength | Key source, date, URL |
|---|---|---|---|
| Identity | mitfa is the Danio rerio MITF ortholog historically named nacre; it is distinct from the duplicated paralog mitfb. This matches UniProt Q9PWC2 and the supplied organism. | Direct zebrafish genetics and comparative annotation; strong. | Miyadai et al., 11 Sep 2023, Development (miyadai2023ageneregulatory pages 1-2) |
| Molecular function and domains | Mitfa is a MiT/TFE-family basic helix–loop–helix leucine-zipper transcription factor. Its basic region binds DNA and its HLH/zipper region mediates homo- or heterodimerization; the supplied bHLH, MiT/TFE-N and MiT/TFE-C annotations are concordant. | Family/structural conservation plus zebrafish phenotype; DNA-recognition and partner details are principally general MiT/TFE inference, not fully demonstrated for Q9PWC2 in vivo. | Steingrímsson et al., Dec 2004, Annual Review of Genetics (steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8); Curran et al., 13 Jun 2009, Developmental Biology (curran2009foxd3controlsmelanophore pages 1-2) |
| Cellular localization | Mitfa performs its primary function in the nucleus, where it regulates transcription at E-box-like elements. | Nuclear localization is well established for MITF/MiT-TFE factors but is mainly family-level inference here; no retrieved study directly mapped endogenous Q9PWC2 protein localization. | Steingrímsson et al., Dec 2004, Annual Review of Genetics (steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8) |
| Upstream regulators | Sox10 and Wnt/TCF-LEF positively regulate mitfa; Foxd3 directly represses its promoter and restricts the melanophore-fated domain. Pax3 and Sox10 cooperate: co-expression induced ectopic mitfa in 30/38 embryos, whereas either alone did not. | Direct zebrafish promoter, mutant, injection and expression evidence; strong. | Curran et al., 13 Jun 2009, Developmental Biology (curran2009foxd3controlsmelanophore pages 1-2); Miyadai et al., 11 Sep 2023, Development (miyadai2023ageneregulatory pages 7-8) |
| Downstream transcriptional outputs | Mitfa activates the melanophore differentiation program. dct is the clearest zebrafish-supported output: mitfa overexpression induced ectopic dct in 22/23 embryos. tyr, tyrp1, kita and bcl2 are biologically plausible MITF outputs, but their direct regulation by zebrafish Q9PWC2 is less completely demonstrated in the retrieved evidence. | dct: direct/functional zebrafish evidence, strong. Other targets: conserved MITF literature or pathway placement, moderate/inferred. | Miyadai et al., 11 Sep 2023, Development (miyadai2023ageneregulatory pages 7-8, miyadai2023ageneregulatory pages 1-2); Curran et al., 13 Jun 2009, Developmental Biology (curran2009foxd3controlsmelanophore pages 1-2) |
| Loss-of-function phenotype | Homozygous mitfa/nacre mutants lack neural-crest-derived body melanophores throughout life, with extensive loss of melanophore markers. Rescue by ectopic mitfa supports a primary role in lineage specification and differentiation rather than pigment chemistry alone. | Direct zebrafish mutant and rescue evidence; very strong. | Miyadai et al., 11 Sep 2023, Development (miyadai2023ageneregulatory pages 1-2); Curran et al., 13 Jun 2009, Developmental Biology (curran2009foxd3controlsmelanophore pages 1-2) |
| Xanthophore role | Ordinary mitfa loss does not eliminate xanthophores, but their development can be abnormal. Mitfa cooperates with Pax7 and partially redundantly with Tfec: Mitfa plus Pax7 induced the xanthophore marker gch2 in 26/31 embryos, and mitfa;tfec double mutants lack xanthophores. Mitfa is therefore not exclusively melanophore-specific. | Direct zebrafish overexpression and genetic-interaction evidence; moderate-to-strong. | Miyadai et al., 11 Sep 2023, Development (miyadai2023ageneregulatory pages 7-8, miyadai2023ageneregulatory pages 1-2); Korzeniwsky et al., Mar 2025, Pigment Cell & Melanoma Research (korzeniwsky2025dominantnegativemitf pages 10-11) |
| RPE distinction | Unlike the neural-crest melanophore lineage, zebrafish retinal pigment epithelium develops and pigments normally after loss of mitfa, mitfb or both. Otx factors are required upstream, and mitfa can induce retinal pigmentation when misexpressed, showing competence but not normal necessity. | Direct double-mutant, histological and misexpression evidence; strong. | Lane & Lister, 5 Nov 2012, PLOS ONE (lane2012otxbutnot pages 1-2) |
| Regeneration | Unpigmented adult skin progenitors express mitfa and regenerate melanocytes by direct differentiation or asymmetric division. A 2023 study resolved 5,619 mitfa⁺aox5-low cells and found KIT–RAS/MAPK signaling essential for these routes; kita loss caused a >8-fold decrease in direct differentiation and a 2-fold decrease in asymmetric division. | Direct lineage imaging, mutants and scRNA-seq; strong. | Frantz et al., 6 Apr 2023, eLife (frantz2023pigmentcellprogenitor pages 9-11, frantz2023pigmentcellprogenitor pages 5-7, frantz2023pigmentcellprogenitor pages 1-2) |
| 2024 mitfa-Cas9 application | Cas9 was knocked into endogenous mitfa exon 2 to preserve native lineage regulation and enable melanocyte-specific gene disruption. The system targeted albino, sox10, tuba1a and ptena/b and modeled BRAF^V600E melanoma with tp53/pten loss; it remains a preprint implementation rather than peer-reviewed functional annotation. | Endogenous knock-in and in-vivo proof of concept; promising but preprint-level. | Perlee et al., initially posted 22 Mar 2024, bioRxiv (perlee2024identifyinginvivo pages 1-3) |
Table: Evidence table for zebrafish mitfa/Q9PWC2, separating direct zebrafish findings from MiT/TFE-family inference. It summarizes molecular function, lineage roles, localization, pathways, regeneration and recent experimental applications.
Zebrafish underwent teleost genome duplication and retained two MITF-related genes, mitfa/nacre and mitfb. The target of this report is specifically mitfa, not mitfb. The classical mitfa loss-of-function allele mitfa^w2, also called nacre, eliminates neural-crest-derived melanophores throughout life. This gene identity, organism and phenotype align with UniProt Q9PWC2 as supplied by the user. (steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8, miyadai2023ageneregulatory pages 1-2)
Mitfa belongs to the MiT/TFE family of bHLH-leucine-zipper transcription factors. The basic region mediates sequence-specific DNA contact, whereas the helix–loop–helix and leucine-zipper region mediates dimerization. MiT/TFE proteins recognize E-box/M-box-like motifs, including CATGTG-class elements, and can form homodimers or heterodimers with related Tfe3, Tfeb or Tfec proteins. These biochemical details are strongly established for conserved MiT/TFE proteins, but the retrieved literature does not demonstrate every binding preference or partner directly for endogenous Q9PWC2 in zebrafish. The supplied DUF3371/PF11851 and MiT/TFE terminal annotations are therefore structurally consistent, while their separate zebrafish-specific biochemical functions remain incompletely resolved. (steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8)
Mitfa is a DNA-binding transcriptional activator and lineage-determining regulator. Its normal site of action is the nucleus of pigment-lineage precursors and differentiated pigment cells. Nuclear localization follows from the conserved MiT/TFE mechanism and transcriptional function; however, a dedicated endogenous-Q9PWC2 localization experiment was not identified among the retrieved zebrafish studies. Thus, nuclear localization is high-confidence family-level inference supported by promoter regulation and transcriptional phenotypes, rather than a newly demonstrated localization for this accession. (steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8)
The clearest zebrafish-supported downstream output is dct, encoding dopachrome tautomerase, a melanogenesis-associated protein and melanophore marker. In a 2023 study, mitfa overexpression induced ectopic dct expression in 22 of 23 embryos, supporting a functional Mitfa→dct relationship. Earlier work places Mitf upstream of pigmentation and survival genes including tyr, tyrp1, kita and bcl2, but the retrieved evidence does not establish direct endogenous Mitfa occupancy at every one of these zebrafish loci. They should therefore be regarded as supported pathway outputs or conserved MITF targets rather than uniformly proven direct Q9PWC2 targets. (miyadai2023ageneregulatory pages 7-8, curran2009foxd3controlsmelanophore pages 1-2)
Mitfa is not a pigment-synthesis enzyme itself. Instead, it activates the transcriptional machinery that generates melanophores and their melanin-producing apparatus. The complete loss of body melanophores in mutants—rather than merely production of unpigmented cells—shows that its primary role lies upstream at lineage specification, differentiation and cell-state maintenance. (miyadai2023ageneregulatory pages 1-2, curran2009foxd3controlsmelanophore pages 1-2)
Sox10 is a major positive input into the mitfa promoter. Forced mitfa expression can rescue melanophore differentiation in zebrafish sox10 mutants, indicating that a major pigment-lineage function of Sox10 is activation of mitfa. Canonical Wnt/TCF-LEF signaling also promotes mitfa transcription and melanophore fate. (lapedriza2015generegulatorynetwork pages 20-23, curran2009foxd3controlsmelanophore pages 1-2)
Recent work refined this model by showing cooperation between Pax3 and Sox10. At 6 hours post-fertilization, neither factor alone induced endogenous mitfa, whereas co-injection induced ectopic expression in 30/38 embryos. This supports a combinatorial regulatory architecture rather than a single-factor master switch. Pax3 loss delays mitfa expression, while related Pax7 factors can partly compensate or redirect the output toward other pigment-cell fates. (miyadai2023ageneregulatory pages 7-8)
Foxd3 restricts the melanophore-fated domain. Mitfa is expressed in Foxd3-negative neural-crest cells; foxd3 mutants expand the spatial domain of mitfa. Reporter assays and embryo injections support direct repression of the mitfa promoter by Foxd3. This provides a mechanistic fate-choice model: cells retaining Foxd3 suppress Mitfa and avoid melanophore specification, whereas release from Foxd3 repression permits the Mitfa program. (curran2009foxd3controlsmelanophore pages 1-2)
Although Mitfa is often termed a “master regulator,” current expert interpretation is more nuanced. Most neural-crest cells may transiently activate mitfa, yet only approximately half subsequently activate melanophore markers such as dct. Cell fate therefore depends on Mitfa dosage and timing together with Sox10, Pax3/7, Foxd3, Tfec and extracellular signaling, rather than Mitfa expression alone. (lapedriza2015generegulatorynetwork pages 20-23)
The strongest functional evidence is the nacre phenotype: homozygous mitfa mutants lack body melanophores from embryonic through adult stages and lack extensive sets of melanophore markers. Ectopic Mitfa can confer melanophore characteristics, and expression in sox10 mutants restores differentiation. Together, necessity, sufficiency and rescue experiments establish Mitfa as the central transcriptional regulator of the neural-crest melanophore lineage. (curran2009foxd3controlsmelanophore pages 1-2, miyadai2023ageneregulatory pages 1-2)
Mitfa is not strictly melanophore-specific. Ordinary mitfa loss permits xanthophores to form, although abnormalities have been reported. In 2023 experiments, Mitfa and Pax7 cooperatively induced the xanthophore marker gch2 in 26/31 embryos, while Pax7 alone did not. Conversely, Pax7 suppressed Mitfa-driven dct induction in 18/18 embryos, illustrating how combinatorial transcription-factor activity can redirect Mitfa output from melanophore toward xanthophore programs. (miyadai2023ageneregulatory pages 7-8, miyadai2023ageneregulatory pages 1-2)
Genetic evidence also supports partial redundancy with Tfec. mitfa;tfec double mutants lack xanthophores from embryonic through adult stages, whereas single-mutant phenotypes are less severe. A dominant-negative DNA-binding-domain allele reported in 2025 eliminated both melanophores and xanthophores and impaired precursor survival, indicating that dominant interference with related MiT/TFE complexes can be broader than simple mitfa null loss. This 2025 result is informative but lies outside the requested 2023–2024 priority window. (korzeniwsky2025dominantnegativemitf pages 10-11, korzeniwsky2025dominantnegativemitf pages 1-3)
Mitfa’s requirement is tissue-specific. Zebrafish carrying mutations in mitfa, mitfb, or both retained normal RPE pigmentation, development and retinal lamination. Otx factors are required for proper mitfa/mitfb expression, but the Mitf factors are not required for Otx expression. Misexpressed mitfa can induce retinal pigmentation, demonstrating melanogenic competence without normal developmental necessity. The best annotation is therefore: Mitfa is essential for neural-crest-derived melanophores but dispensable for normal zebrafish neuroepithelial RPE development, presumably because other regulatory factors provide the necessary activity there. (lane2012otxbutnot pages 1-2)
Adult zebrafish skin contains unpigmented mitfa-positive melanocyte progenitors intermingled with mature melanocytes. After melanocyte ablation, these cells either differentiate directly, divide asymmetrically to produce one differentiating daughter, or divide symmetrically to replenish the progenitor pool. Wnt activity precedes differentiation, while a 2023 eLife study identified KIT–RAS/MAPK signaling as a major regulator of both direct differentiation and asymmetric division. (frantz2023pigmentcellprogenitor pages 1-2)
The 2023 study resolved 5,619 mitfa-positive, aox5-low cells into melanocytes and several progenitor/intermediate states. Pseudotime analysis found two routes from an MP-0 progenitor state to melanocytes: one through a direct-differentiation intermediate and another through MP-1 and cycling-differentiation states. Mature states expressed genes such as tyrp1b and pmela, whereas early progenitors expressed sox4a and sox10. (frantz2023pigmentcellprogenitor pages 5-7)
Loss of kita produced a greater than eightfold decrease in progenitors undergoing direct differentiation and an approximately twofold decrease in asymmetric divisions. The study sequenced 24,724 transcriptomes from regenerating kita mutant mitfa-reporter cells; phenotype quantification used wild-type n=10, kita loss-of-function n=9 and kitlga loss-of-function n=11 fish. These data position mitfa-positive cells as the lineage substrate on which KIT–MAPK and Wnt signals act, rather than proving that KIT directly modifies Mitfa protein. (frantz2023pigmentcellprogenitor pages 9-11)
The accessibility and visible pigmentation of zebrafish make mitfa reporters useful for tracking progenitor activation, differentiation and tissue repair in vivo. The regeneration model has relevance to stem-cell biology and hypopigmentation disorders such as vitiligo, although direct clinical translation has not yet occurred. The 2023 single-cell atlas offers a quantitative framework for testing regenerative signals and candidate compounds. (frantz2023pigmentcellprogenitor pages 9-11, frantz2023pigmentcellprogenitor pages 1-2)
Mitfa regulatory sequences are widely used to restrict oncogene or genome-editing activity to melanocyte-lineage cells. This reflects endogenous lineage specificity and allows researchers to distinguish tumor-cell-autonomous effects from systemic developmental effects. Because MITF state is associated with melanoma differentiation, proliferation and invasion, these models are useful for studying phenotype switching; nevertheless, human MITF oncology should not be assumed to reproduce every zebrafish Mitfa mechanism. (perlee2024identifyinginvivo pages 1-3)
A 2024 bioRxiv study knocked Cas9 into exon 2 of the endogenous mitfa locus, preserving native regulatory control and targeting the only exon shared by three protein-coding transcripts. Mitfa expression was detectable by approximately 18 hpf and was prominent in melanocytes, xanthophores and their progenitors. The platform disrupted albino, sox10, tuba1a and ptena/b selectively in the pigment lineage and generated melanomas by combining melanocyte-restricted tp53 and ptena/b loss with BRAF^V600E. Sox10 disruption reduced tumor initiation but yielded rare invasive Sox9-high tumors, illustrating how in-vivo dependencies may differ from cell-culture screens. Because this work remains a preprint, its conclusions should be treated as promising rather than fully validated. Publication record: initially posted 22 March 2024, DOI/URL: https://doi.org/10.1101/2024.03.22.586101. (perlee2024identifyinginvivo pages 1-3)
High-confidence direct zebrafish annotation: Mitfa is a nuclear-lineage transcription factor essential for body melanophore specification and differentiation; it acts downstream of Sox10/Pax3 and Wnt inputs, is restricted by Foxd3, activates dct, contributes combinatorially to xanthophore programs, and marks adult regenerative melanocyte progenitors. (miyadai2023ageneregulatory pages 7-8, miyadai2023ageneregulatory pages 1-2, frantz2023pigmentcellprogenitor pages 1-2, curran2009foxd3controlsmelanophore pages 1-2)
High-confidence negative annotation: Mitfa is not an enzyme, transporter, secreted ligand or structural protein. It is also not required—alone or together with Mitfb—for normal zebrafish RPE pigmentation and morphogenesis under the tested conditions. (lane2012otxbutnot pages 1-2)
Inference requiring caution: Exact endogenous Q9PWC2 DNA-binding motifs, dimer partners, post-translational controls and nuclear trafficking have not all been measured directly in zebrafish. CATGTG/E-box recognition, MiT/TFE heterodimerization and many target-gene assignments are strongly supported by conserved MITF-family biology but should be labeled as orthology-based inference where zebrafish-specific occupancy or biochemistry is absent. (steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8)
Danio rerio Mitfa/Q9PWC2 is a nuclear MiT/TFE-family bHLH-leucine-zipper transcription factor that converts developmental and regenerative signals into pigment-cell gene expression. Its principal physiological function is to specify and differentiate neural-crest-derived melanophores by activating melanogenic and lineage-maintenance programs, with experimentally supported output through dct. It also participates, in combination with Pax7 and Tfec, in xanthophore development and marks adult progenitors whose differentiation is controlled by Wnt and KIT–RAS/MAPK signaling. Its function is dispensable for normal zebrafish RPE development, demonstrating strong lineage and tissue-context specificity.
References
(steingrimsson2004melanocytesandthemicrophthalmiatranscription pages 6-8): Eiríkur Steingrímsson, Neal G. Copeland, and Nancy A. Jenkins. Melanocytes and themicrophthalmiatranscription factor network. Dec 2004. URL: https://doi.org/10.1146/annurev.genet.38.072902.092717, doi:10.1146/annurev.genet.38.072902.092717. This article has 1064 citations and is from a domain leading peer-reviewed journal.
(miyadai2023ageneregulatory pages 1-2): Motohiro Miyadai, Hiroyuki Takada, Akiko Shiraishi, Tetsuaki Kimura, Ikuko Watakabe, Hikaru Kobayashi, Yusuke Nagao, Kiyoshi Naruse, Shin-ichi Higashijima, Takashi Shimizu, Robert N. Kelsh, Masahiko Hibi, and Hisashi Hashimoto. A gene regulatory network combining pax3/7, sox10 and mitf generates diverse pigment cell types in medaka and zebrafish. Development (Cambridge, England), Oct 2023. URL: https://doi.org/10.1242/dev.202114, doi:10.1242/dev.202114. This article has 52 citations.
(lane2012otxbutnot pages 1-2): Brandon M. Lane and James A. Lister. Otx but not mitf transcription factors are required for zebrafish retinal pigment epithelium development. PLoS ONE, 7:e49357, Nov 2012. URL: https://doi.org/10.1371/journal.pone.0049357, doi:10.1371/journal.pone.0049357. This article has 56 citations and is from a peer-reviewed journal.
(curran2009foxd3controlsmelanophore pages 1-2): Kevin Curran, David W. Raible, and James A. Lister. Foxd3 controls melanophore specification in the zebrafish neural crest by regulation of mitf. Developmental biology, 332 2:408-17, Aug 2009. URL: https://doi.org/10.1016/j.ydbio.2009.06.010, doi:10.1016/j.ydbio.2009.06.010. This article has 129 citations and is from a peer-reviewed journal.
(miyadai2023ageneregulatory pages 7-8): Motohiro Miyadai, Hiroyuki Takada, Akiko Shiraishi, Tetsuaki Kimura, Ikuko Watakabe, Hikaru Kobayashi, Yusuke Nagao, Kiyoshi Naruse, Shin-ichi Higashijima, Takashi Shimizu, Robert N. Kelsh, Masahiko Hibi, and Hisashi Hashimoto. A gene regulatory network combining pax3/7, sox10 and mitf generates diverse pigment cell types in medaka and zebrafish. Development (Cambridge, England), Oct 2023. URL: https://doi.org/10.1242/dev.202114, doi:10.1242/dev.202114. This article has 52 citations.
(korzeniwsky2025dominantnegativemitf pages 10-11): Katia G. Korzeniwsky, Pietro L.H. de Mello, Yipeng Liang, McKenna Feltes, Steven A. Farber, and David M. Parichy. Dominant negative mitf allele impacts melanophore and xanthophore development and reveals collaborative interactions with tfec in zebrafish chromatophore lineages. Pigment Cell & Melanoma Research, Mar 2025. URL: https://doi.org/10.1111/pcmr.70009, doi:10.1111/pcmr.70009. This article has 9 citations and is from a domain leading peer-reviewed journal.
(frantz2023pigmentcellprogenitor pages 9-11): William Tyler Frantz, Sharanya Iyengar, James Neiswender, Alyssa Cousineau, René Maehr, and Craig J Ceol. Pigment cell progenitor heterogeneity and reiteration of developmental signaling underlie melanocyte regeneration in zebrafish. eLife, Apr 2023. URL: https://doi.org/10.7554/elife.78942, doi:10.7554/elife.78942. This article has 12 citations and is from a domain leading peer-reviewed journal.
(frantz2023pigmentcellprogenitor pages 5-7): William Tyler Frantz, Sharanya Iyengar, James Neiswender, Alyssa Cousineau, René Maehr, and Craig J Ceol. Pigment cell progenitor heterogeneity and reiteration of developmental signaling underlie melanocyte regeneration in zebrafish. eLife, Apr 2023. URL: https://doi.org/10.7554/elife.78942, doi:10.7554/elife.78942. This article has 12 citations and is from a domain leading peer-reviewed journal.
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(perlee2024identifyinginvivo pages 1-3): S. Perlee, Yilun Ma, Miranda V. Hunter, Jacob B. Swanson, Nelly M. Cruz, Zhitao Ming, Julia Xia, T. Lionnet, M. McGrail, and Richard M. White. Identifying in vivo genetic dependencies of melanocyte and melanoma development. bioRxiv, Mar 2024. URL: https://doi.org/10.1101/2024.03.22.586101, doi:10.1101/2024.03.22.586101. This article has 0 citations.
(lapedriza2015generegulatorynetwork pages 20-23): A Lapedriza. Gene regulatory network of melanocyte development. Unknown journal, 2015.
(korzeniwsky2025dominantnegativemitf pages 1-3): Katia G. Korzeniwsky, Pietro L.H. de Mello, Yipeng Liang, McKenna Feltes, Steven A. Farber, and David M. Parichy. Dominant negative mitf allele impacts melanophore and xanthophore development and reveals collaborative interactions with tfec in zebrafish chromatophore lineages. Pigment Cell & Melanoma Research, Mar 2025. URL: https://doi.org/10.1111/pcmr.70009, doi:10.1111/pcmr.70009. This article has 9 citations and is from a domain leading peer-reviewed journal.