Talk:Neural Crest - Melanocyte Development
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Cite this page: Hill, M.A. (2024, April 19) Embryology Neural Crest - Melanocyte Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_Crest_-_Melanocyte_Development |
2017
The patterns of birthmarks suggest a novel population of melanocyte precursors arising around the time of gastrulation
Pigment Cell Melanoma Res. 2017 Sep 23. doi: 10.1111/pcmr.12645. [Epub ahead of print]
Kinsler VA1,2, Larue L3,4,5.
Abstract
Systematic work in the mouse and chicken has mapped out two neural crest-derived pathways of melanocyte precursor migration. With these in mind, this study reappraises the patterns of congenital pigmentary disorders in humans, and identifies three recurrent patterns consistent across genetically-different diseases. Only two of these are seen in diseases known to be melanocyte cell-autonomous. The segmental pattern correlates well with the classical dorsolateral population from animal studies, demonstrating respect of the midline, craniocaudal axial mixing, unilateral migration and involvement of key epidermally-derived structures. Importantly however, the melanocyte precursors responsible for the non-segmental pattern, which demonstrates circular, bilateral migration centred on the midline, and not involving key epidermally-derived structures, have not been identified previously. We propose that this population originates around the time of gastrulation, most likely within the mesoderm, and ultimately resides within the dermis. Whether it contributes to mature melanocytes in non-disease states is not known, however parallels with the patterns of acquired vitiligo would suggest that it does. The third pattern, hypo- or hyper-pigmented fine and whorled Blaschko's lines, is proposed to be non-cell-autonomous. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved. KEYWORDS: Birthmark; Development; Melanoblast; Melanocytic; Migration; Mosaicism; Non-segmental; Pattern; Population; Segmental; Spray can; Vitiligo
PMID: 28940934 DOI: 10.1111/pcmr.12645
2015
The melanocyte lineage in development and disease
Development. 2015 Feb 15;142(4):620-632.
Mort RL1, Jackson IJ2, Patton EE3.
Abstract
Melanocyte development provides an excellent model for studying more complex developmental processes. Melanocytes have an apparently simple aetiology, differentiating from the neural crest and migrating through the developing embryo to specific locations within the skin and hair follicles, and to other sites in the body. The study of pigmentation mutations in the mouse provided the initial key to identifying the genes and proteins involved in melanocyte development. In addition, work on chicken has provided important embryological and molecular insights, whereas studies in zebrafish have allowed live imaging as well as genetic and transgenic approaches. This cross-species approach is powerful and, as we review here, has resulted in a detailed understanding of melanocyte development and differentiation, melanocyte stem cells and the role of the melanocyte lineage in diseases such as melanoma. © 2015. Published by The Company of Biologists Ltd. KEYWORDS: MITF; Melanoma; Neural crest; Stem cells
PMID 25670789
http://dev.biologists.org/content/142/4/620.full?sid=9c0c0b67-790f-42a6-8551-73876896a0d6
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2014
The biology of hyper pigmentation syndromes
Pigment Cell Melanoma Res. 2014 Feb 24. doi: 10.1111/pcmr.12235. [Epub ahead of print]
Speeckaert R1, Van Gele M, Speeckaert MM, Lambert J, van Geel N. Author information
Abstract
Hyperpigmentation is a key feature in a variety of inherited and acquired syndromes. Nonetheless, determining the exact diagnosis only on the clinical phenotype can be challenging, and a detailed search for associated symptoms is often of crucial importance. As pigmentation pathways are regulated by complex signaling transduction cascades (e.g. MSH/cAMP, KIT signaling pathways), the underlying defects leading to elevated melanin production are numerous. With regard to treatment, limited therapeutic options exist, each with specific side effects. In acquired hyperpigmentation, the melanin deposition may, however, be reversible after adequate therapy of the underlying disorder or even disappear spontaneously. In this review, we provide an overview of the biology of hyperpigmentation syndromes classified according to the main underlying defect that deregulates physiological melanogenesis. The identification of novel genes or key players involved in hyperpigmentary disorders is becoming increasingly important in view of the development of safer and more efficient treatments. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. KEYWORDS: hyperpigmentation, melanin, melanocyte, pigmentation pathway, syndrome
PMID 24612852
2013
The EJC component Magoh regulates proliferation and expansion of neural crest-derived melanocytes
Dev Biol. 2013 Mar 15;375(2):172-81. doi: 10.1016/j.ydbio.2013.01.004. Epub 2013 Jan 18.
Silver DL1, Leeds KE, Hwang HW, Miller EE, Pavan WJ. Author information
Abstract
Melanoblasts are a population of neural crest-derived cells that generate the pigment-producing cells of our body. Defective melanoblast development and function underlies many disorders including Waardenburg syndrome and melanoma. Understanding the genetic regulation of melanoblast development will help elucidate the etiology of these and other neurocristopathies. Here we demonstrate that Magoh, a component of the exon junction complex, is required for normal melanoblast development. Magoh haploinsufficient mice are hypopigmented and exhibit robust genetic interactions with the transcription factor, Sox10. These phenotypes are caused by a marked reduction in melanoblast number beginning at mid-embryogenesis. Strikingly, while Magoh haploinsufficiency severely reduces epidermal melanoblasts, it does not significantly affect the number of dermal melanoblasts. These data indicate Magoh impacts melanoblast development by disproportionately affecting expansion of epidermal melanoblast populations. We probed the cellular basis for melanoblast reduction and discovered that Magoh mutant melanoblasts do not undergo increased apoptosis, but instead are arrested in mitosis. Mitotic arrest is evident in both Magoh haploinsufficient embryos and in Magoh siRNA treated melanoma cell lines. Together our findings indicate that Magoh-regulated proliferation of melanoblasts in the dermis may be critical for production of epidermally-bound melanoblasts. Our results point to a central role for Magoh in melanocyte development. Copyright © 2013 Elsevier Inc. All rights reserved. PMID 23333945
Modeling melanoblast development
Cell Mol Life Sci. 2013 Mar;70(6):1067-79. doi: 10.1007/s00018-012-1112-4. Epub 2012 Aug 23.
Larue L1, de Vuyst F, Delmas V. Author information
Abstract
Melanoblasts are a particular type of cell that displays extensive cellular proliferation during development to contribute to the skin. There are only a few melanoblast founders, initially located just dorsal to the neural tube, and they sequentially colonize the dermis, epidermis, and hair follicles. In each compartment, melanoblasts are exposed to a wide variety of developmental cues that regulate their expansion. The colonization of the dermis and epidermis by melanoblasts involves substantial proliferation to generate thousands of cells or more from a few founders within a week of development. This review addresses the cellular and molecular events occurring during melanoblast development. We focus on intrinsic and extrinsic factors that control melanoblast proliferation. We also present a robust mathematical model for estimating the doubling-time of dermal and epidermal melanoblasts for all coat color phenotypes from black to white.
PMID 22915137
2011
Generation of human melanocytes from induced pluripotent stem cells
PLoS One. 2011 Jan 13;6(1):e16182.
Ohta S, Imaizumi Y, Okada Y, Akamatsu W, Kuwahara R, Ohyama M, Amagai M, Matsuzaki Y, Yamanaka S, Okano H, Kawakami Y. Division of Cellular Signaling, Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
Abstract
Epidermal melanocytes play an important role in protecting the skin from UV rays, and their functional impairment results in pigment disorders. Additionally, melanomas are considered to arise from mutations that accumulate in melanocyte stem cells. The mechanisms underlying melanocyte differentiation and the defining characteristics of melanocyte stem cells in humans are, however, largely unknown. In the present study, we set out to generate melanocytes from human iPS cells in vitro, leading to a preliminary investigation of the mechanisms of human melanocyte differentiation. We generated iPS cell lines from human dermal fibroblasts using the Yamanaka factors (SOX2, OCT3/4, and KLF4, with or without c-MYC). These iPS cell lines were subsequently used to form embryoid bodies (EBs) and then differentiated into melanocytes via culture supplementation with Wnt3a, SCF, and ET-3. Seven weeks after inducing differentiation, pigmented cells expressing melanocyte markers such as MITF, tyrosinase, SILV, and TYRP1, were detected. Melanosomes were identified in these pigmented cells by electron microscopy, and global gene expression profiling of the pigmented cells showed a high similarity to that of human primary foreskin-derived melanocytes, suggesting the successful generation of melanocytes from iPS cells. This in vitro differentiation system should prove useful for understanding human melanocyte biology and revealing the mechanism of various pigment cell disorders, including melanoma.
PMID 21249204
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3020956
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016182
2008
The secreted metalloprotease ADAMTS20 is required for melanoblast survival
PLoS Genet. 2008 Feb 29;4(2):e1000003. doi: 10.1371/journal.pgen.1000003.
Silver DL1, Hou L, Somerville R, Young ME, Apte SS, Pavan WJ. Author information
Abstract
ADAMTS20 (Adisintegrin-like and metalloprotease domain with thrombospondin type-1 motifs) is a member of a family of secreted metalloproteases that can process a variety of extracellular matrix (ECM) components and secreted molecules. Adamts20 mutations in belted (bt) mice cause white spotting of the dorsal and ventral torso, indicative of defective neural crest (NC)-derived melanoblast development. The expression pattern of Adamts20 in dermal mesenchymal cells adjacent to migrating melanoblasts led us to initially propose that Adamts20 regulated melanoblast migration. However, using a Dct-LacZ transgene to track melanoblast development, we determined that melanoblasts were distributed normally in whole mount E12.5 bt/bt embryos, but were specifically reduced in the trunk of E13.5 bt/bt embryos due to a seven-fold higher rate of apoptosis. The melanoblast defect was exacerbated in newborn skin and embryos from bt/bt animals that were also haploinsufficient for Adamts9, a close homolog of Adamts20, indicating that these metalloproteases functionally overlap in melanoblast development. We identified two potential mechanisms by which Adamts20 may regulate melanoblast survival. First, skin explant cultures demonstrated that Adamts20 was required for melanoblasts to respond to soluble Kit ligand (sKitl). In support of this requirement, bt/bt;Kit(tm1Alf)/+ and bt/bt;Kitl(Sl)/+ mice exhibited synergistically increased spotting. Second, ADAMTS20 cleaved the aggregating proteoglycan versican in vitro and was necessary for versican processing in vivo, raising the possibility that versican can participate in melanoblast development. These findings reveal previously unrecognized roles for Adamts proteases in cell survival and in mediating Kit signaling during melanoblast colonization of the skin. Our results have implications not only for understanding mechanisms of NC-derived melanoblast development but also provide insights on novel biological functions of secreted metalloproteases.
PMID 18454205
