The Regulation of Normal Melanocyte Proliferation

2000 ◽  
Vol 13 (1) ◽  
pp. 4-14 ◽  
Author(s):  
Ruth Halaban
Keyword(s):  
2003 ◽  
Vol 16 (4) ◽  
pp. 407-410 ◽  
Author(s):  
Sophia Jule ◽  
Philippe Bosse ◽  
Giorgia Egidy ◽  
Jean-Jacques Panthier
Keyword(s):  
Pig Skin ◽  

Genetics ◽  
1994 ◽  
Vol 138 (2) ◽  
pp. 491-497
Author(s):  
K J Moore ◽  
D A Swing ◽  
N G Copeland ◽  
N A Jenkins

Abstract The murine dilute suppressor gene (dsu) suppresses the coat-color phenotype of three pigment mutations, dilute (d), ashen (ash) and leaden (ln), that each produce adendritic melanocytes. Suppression is due to the ability of dsu to partially restore (ash and ln), or almost completely restore (d), normal melanocyte morphology. While the ash and ln gene products have yet to be identified, the d gene encodes a novel myosin heavy chain (myosin 12), which is speculated to be necessary for the elaboration, maintenance, and/or function of melanocyte cell processes. To begin to discriminate between different models of dsu action, we have produced aggregation chimeras between mice homozygous for dsu and mice homozygous for d to determine if dsu acts cell autonomously or cell nonautonomously. In addition, we have further refined the map location of dsu in order to examine a number of possible dsu candidate genes mapping in the region and to provide a genetic basis for the positional cloning of dsu.


Author(s):  
María José Salazar-Nicholls ◽  
Francisca Hervas ◽  
Sofía Isabel Muñoz-Tobar ◽  
Ana-Belén Carrillo ◽  
Heisel Ricaurte ◽  
...  

The adaptive role of amphibian oocyte melanic pigmentation and its molecular control are still elusive. Here we present evidence of a polymorphism in egg pigmentation in the emerald glass frog Espadarana prosoblepon. In Ecuadorian natural populations of this species, females can lay dark brown or pale eggs that develop into normal pigmented tadpoles and adults. This trait is a sex-limited phenotype that is inherited like a recessive allele that we called pale eggs like (pel). The pel phenotype is exclusive of oocyte cortical melanic pigmentation, which is reduced in comparison to wild type (wt) dark pigmented oocytes. Consequently, pel early embryos are paler in appearance, with reduced melanic pigmentation distributed to early blastomeres and embryonic ectoderm. However, these embryos form normal melanocyte derived pigmentation. Finally, we discuss the origin of this polymorphism and propose the use of E. prosoblepon as a model to study the adaptive role of egg pigmentation.


Development ◽  
2000 ◽  
Vol 127 (17) ◽  
pp. 3715-3724 ◽  
Author(s):  
J.F. Rawls ◽  
S.L. Johnson

Fin regeneration in adult zebrafish is accompanied by re-establishment of the pigment stripes. To understand the mechanisms underlying fin stripe regeneration and regulation of normal melanocyte stripe morphology, we investigated the origins of melanocytes in the regenerating fin and their requirement for the kit receptor tyrosine kinase. Using pre-existing melanin as a lineage tracer, we show that most fin regeneration melanocytes develop from undifferentiated precursors, rather than from differentiated melanocytes. Mutational analysis reveals two distinct classes of regeneration melanocytes. First, an early regeneration class develops dependent on kit function. In the absence of kit function and kit-dependent melanocytes, a second class of melanocytes develops at later stages of regeneration. This late kit-independent class of regeneration melanocytes has little or no role in wild-type fin stripe development, thus revealing a secondary mode for regulation of fin stripes. Expression of melanocyte markers in regenerating kit mutant fins suggests that kit normally acts after mitf and before dct to promote development of the primary kit-dependent melanocytes. kit-dependent and kit-independent melanocytes are also present during fin stripe ontogeny in patterns similar to those observed during regeneration.


1982 ◽  
Vol 156 (6) ◽  
pp. 1755-1766 ◽  
Author(s):  
A N Houghton ◽  
M Eisinger ◽  
A P Albino ◽  
J G Cairncross ◽  
L J Old

The surface antigens of melanocytes from newborn and adult skin have been analyzed with monoclonal antibodies detecting cell surface antigens of malignant melanoma. Antigenic markers that distinguish early, intermediate, and mature stages in melanocyte differentiation have been defined. The characteristics of the normal melanocyte precursor have been inferred from the features of melanomas that express early markers of melanocyte differentiation. A rudimentary surface antigen map of cells undergoing melanocyte differentiation and a new classification of melanomas based on the expression of melanocyte differentiation antigens are proposed.


2020 ◽  
Vol 1 (1) ◽  
pp. 33-47
Author(s):  
Monica Neagu ◽  
◽  
Carolina Constantin ◽  
Ayse Basak Engin ◽  
Iulia Popescu ◽  
...  

The largest organ with immune function, the skin, has complex structure and various physiological functions. Cells comprising this complex structure sustain various processes and have proteomic/transcriptomic/genomic patterns that would subside to developing a specific function in a specific moment of time and in a defined space. Within the complex skin structure melanocyte is one of the cell types that is involved in skin’s main functions. In the process of normal melanocyte transformation into a neoplastic cell there are several stages that are favored by a protumor inflammatory milieu. A tumorigenesis-friendly environment would increase cell’s genetic instability that will further lead to tumorigenesis and additionally to metastasis. In the environment, immune cells and immune-related molecules seminally contribute to the inflammatory landscape. Melanomagenesis is not a straight forward process. In order to take place, various factors need to collide, environmental, genetic, and immune factors must conjoint. Melanomas are heterogeneous and the transformed melanocyte has various genetic alterations, these mutations being specific to the site, to the degree of UV exposure, and/or specific for the genetic make-up of the host’s organism. This variability suggests that melanoma has more than one causal pathway. Within our paper we will snapshot the cellular identity of normal melanocyte, through benign transformed melanocyte up to a full blown tumorigenesis. Factors that are triggering these transformations(s) will be briefly highlighted.


Genetics ◽  
1988 ◽  
Vol 119 (4) ◽  
pp. 933-941
Author(s):  
K J Moore ◽  
D A Swing ◽  
E M Rinchik ◽  
M L Mucenski ◽  
A M Buchberg ◽  
...  

Abstract The murine dilute suppressor gene, dsu, was identified because of its ability to suppress the dilute coat color of mice homozygous for the retrovirally induced allele (dv) of the dilute locus (d). dsu is unlinked to the d locus and has recently been shown to be semidominantly inherited. The dilute phenotype of d/d mice is the consequence of abnormal melanocyte morphology. While wild-type melanocytes are dendritic, d/d melanocytes are adendritic. dsu apparently suppresses the dilute phenotype by restoring normal melanocyte morphology. In addition to d, two other loci, ashen (ash) and leaden (ln), have been identified that produce a diluted coat color associated with adendritic melanocytes. Interestingly, d and ash are closely linked on chromosome 9 while dsu and ln are located on chromosome 1. In experiments described here, we present genetic mapping data between ash and d indicating that, despite their identical phenotypes, they are separate genes and are not intragenic complementing alleles of the same locus. We also show that dsu is only loosely linked to ln (approximately 9 cM proximal) and that dsu can suppress, at least partially, the coat color of ln/ln mice and ash/ash mice. The partial suppression of ln and ash coat colors is associated with the partial restoration of normal melanocyte morphology. These studies provide new insights into the mechanism of action of dsu and into the interrelationships between members of a family of pigment genes.


2018 ◽  
Author(s):  
Katherine R. Mattaini ◽  
Mark R. Sullivan ◽  
Allison N. Lau ◽  
Brian P. Fiske ◽  
Roderick T. Bronson ◽  
...  

SUMMARYCopy number gain of the PHGDH gene that encodes the first enzyme of the serine biosynthesis pathway is found in some human cancers, including a subset of melanomas. In order to study the effect of increased PHGDH expression in tissues in vivo, we generated mice harboring a PHGDHtetO allele that allows tissue-specific, doxycycline-inducible PHGDH expression. Tissues and cells derived from PHGDHtetO mice exhibit increased serine biosynthesis. Histological examination of skin tissue from PHGDHtetO mice reveals the presence of melanin granules in anagen II hair follicles, despite the fact that melanin synthesis is normally closely coupled to the hair follicle cycle and does not begin until later in the cycle. This phenotype occurs in the absence of any global change in hair follicle cycle timing. The inappropriate presence of melanin early in the hair follicle cycle following PHGDH expression is also accompanied by increased melanocyte abundance in anagen II skin. Together, these data support a model in which PHGDH expression affects melanocyte proliferation and/or differentiation and may provide insight into how PHGDH expression impacts normal melanocyte biology to promote melanoma.SIGNIFICANCEThe significance behind copy number gain of PHGDH in human cancers is unclear. In this study, we generate a mouse model that mimics PHGDH gene copy number gain and characterize its effect on normal tissues. Increased PHGDH expression yields a phenotype of aberrant melanin production, which indicates that PHGDH expression may play a role in normal melanocyte biology. This result may provide insight into why PHGDH copy number gain is observed in melanoma more frequently than in most other tumor types.


2016 ◽  
Vol 61 ◽  
pp. S109
Author(s):  
D. Sheinboim ◽  
I. Maza ◽  
I. Dror ◽  
J. Hanna ◽  
C. Levy

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