ArticleCurrent biology : CB2007
Zebrafish melanophilin facilitates melanosome dispersion by regulating dynein.
Article in Current biology : CB, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 87 citations in OpenAlex.
- Neuronal microexons modulate arousal via the cAMP-PKA-CREB pathway in zebrafish.Science advances · 2026Article
- Melanin Deficiency Is Associated with Immune Homeostasis in the Critically Endangered Yangtze Sturgeon (International journal of molecular sciences · 2026Article
- STIM1-Mitofusin2 interactions tether mitochondria and melanosome contacts that promote melanosome maturation.Nature communications · 2026Article
- Loss-of-function mutations in the melanocortin-2-receptor (mc2r) lead to skin hyperpigmentation in teleost fish.Scientific reports · 2026Article
- The regenerative period of somatosensory nerves is closed by a DCC signaling axis.PLoS genetics · 2026Article
- Melanophilin regulates dendritogenesis in melanocytes for feather pigmentation.Communications biology · 2024Article
- Identification of Candidate Genes for Red-Eyed (Albinism) Domestic Guppies Using Genomic and Transcriptomic Analyses.International journal of molecular sciences · 2024Article
- Characterising the Effect of Wnt/β-Catenin Signalling on Melanocyte Development and Patterning: Insights from Zebrafish (International journal of molecular sciences · 2023Article
- A frameshift variant in the melanophilin gene is associated with loss of pigment from shed skin in ball pythons (microPublication biology · 2023Article
- Requirement of Zebrafish Adcy3a and Adcy5 in Melanosome Dispersion and Melanocyte Stripe Formation.International journal of molecular sciences · 2022Article
- The Use of Zebrafish as a Non-traditional Model Organism in Translational Pain Research: The Knowns and the Unknowns.Current neuropharmacology · 2022Article
- Single-cell resolution of MET- and EMT-like programs in osteoblasts during zebrafish fin regeneration.iScience · 2022Article
- Epigenetic dynamics shaping melanophore and iridophore cell fate in zebrafish.Genome biology · 2021Article
- Genetic deciphering of the antagonistic activities of the melanin-concentrating hormone and melanocortin pathways in skin pigmentation.PLoS genetics · 2020Article
- Synthetic CRISPR/Cas9 reagents facilitate genome editing and homology directed repair.Nucleic acids research · 2020Article
- Molecular underpinnings of cytoskeletal cross-talk.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Comparative transcriptomics reveals candidate carotenoid color genes in an East African cichlid fish.BMC genomics · 2020Article
- Recent advances in understanding the molecular basis of melanogenesis in melanocytes.F1000Research · 2020Review
- Maintenance of Melanocyte Stem Cell Quiescence by GABA-A Signaling in Larval Zebrafish.Genetics · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundFish melanocytes aggregate or disperse their melanosomes in response to the level of intracellular cAMP. The role of cAMP is to regulate both melanosome travel along microtubules and their transfer between microtubules and actin. The factors that are downstream of cAMP and that directly modulate the motors responsible for melanosome transport are not known. To identify these factors, we are characterizing melanosome transport mutants in zebrafish.
resultsWe report that a mutation (allele j120) in the gene encoding zebrafish melanophilin (Mlpha) interferes with melanosome dispersion downstream of cAMP. Based on mouse genetics, the current model of melanophilin function is that melanophilin links myosin V to melanosomes. The residues responsible for this function are conserved in the zebrafish ortholog. However, if linking myosin V to melanosomes was Mlpha's sole function, elevated cAMP would cause mlpha(j120) mutant melanocytes to hyperdisperse their melanosomes. Yet this is not what we observe. Instead, mutant melanocytes disperse their melanosomes much more slowly than normal and less than halfway to the cell margin. This defect is caused by a failure to suppress minus-end (dynein) motility along microtubules, as shown by tracking individual melanosomes. Disrupting the actin cytoskeleton, which causes wild-type melanocytes to hyperdisperse their melanosomes, does not affect dispersion in mutant melanocytes. Therefore, Mlpha regulates dynein independently of its putative linkage to myosin V.
conclusionsWe propose that cAMP-induced melanosome dispersion depends on the actin-independent suppression of dynein by Mlpha and that Mlpha coordinates the early outward movement of melanosomes along microtubules and their later transfer to actin filaments.
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