From the Crest to the Periphery: Control of Pigment Cell Migration and Lineage Segregation

Erickson, Carol A.

doi:10.1111/j.1600-0749.1993.tb00611.x

Cited by 73 publications

(55 citation statements)

References 114 publications

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“…Signaling through the KIT receptor is critical for the growth, survival, and migration of melanocyte precursors (reviewed by Erickson 1993). It has been shown that both phospholipase C activation and Ca 21 influx are important in supporting KIT-positive cells (Berger 2006).…”

Section: Resultsmentioning

confidence: 99%

Differential Gene Expression of TRPM1, the Potential Cause of Congenital Stationary Night Blindness and Coat Spotting Patterns (LP) in the Appaloosa Horse (Equus caballus)

Bellone

Brooks

Sandmeyer³

et al. 2008

Genetics

152

156

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The appaloosa coat spotting pattern in horses is caused by a single incomplete dominant gene (LP). Homozygosity for LP (LP/LP) is directly associated with congenital stationary night blindness (CSNB) in Appaloosa horses. LP maps to a 6-cM region on ECA1. We investigated the relative expression of two functional candidate genes located in this LP candidate region (TRPM1 and OCA2), as well as three other linked loci (TJP1, MTMR10, and OTUD7A) by quantitative real-time RT-PCR. No large differences were found for expression levels of TJP1, MTMR10, OTUD7A, and OCA2. However, TRPM1 (Transient Receptor Potential Cation Channel, Subfamily M, Member 1) expression in the retina of homozygous appaloosa horses was 0.05% the level found in non-appaloosa horses (R ¼ 0.0005). This constitutes a .1800-fold change (FC) decrease in TRPM1 gene expression in the retina (FC ¼ À1870.637, P ¼ 0.001) of CSNB-affected (LP/LP) horses. TRPM1 was also downregulated in LP/LP pigmented skin (R ¼ 0.005, FC ¼ À193.963, P ¼ 0.001) and in LP/LP unpigmented skin (R ¼ 0.003, FC ¼ À288.686, P ¼ 0.001) and was downregulated to a lesser extent in LP/lp unpigmented skin (R ¼ 0.027, FC ¼ À36.583, P ¼ 0.001). TRP proteins are thought to have a role in controlling intracellular Ca 21 concentration. Decreased expression of TRPM1 in the eye and the skin may alter bipolar cell signaling as well as melanocyte function, thus causing both CSNB and LP in horses.

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Section: Resultsmentioning

confidence: 99%

Differential Gene Expression of TRPM1, the Potential Cause of Congenital Stationary Night Blindness and Coat Spotting Patterns (LP) in the Appaloosa Horse (Equus caballus)

Bellone

Brooks

Sandmeyer³

et al. 2008

Genetics

152

156

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“…In early development, the path taken by pigment cells is likely to be controlled either by a chemotactic mechanism (13)(14)(15)(16)(17) or by guidance cues in the extracellular matrix (18). We postulate that the iridophore cells move chemotactically in response to one of the morphogens, and that the flux of these cells relative to the melanophore cells comprises both a diffusional component caused by random motion and a directed component that results from the tactic response.…”

mentioning

confidence: 99%

Stripe formation in juvenile Pomacanthus explained by a generalized Turing mechanism with chemotaxis

Painter¹,

Maini

Othmer

1999

Proc. Natl. Acad. Sci. U.S.A.

222

164

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Current interest in pattern formation can be traced to a seminal paper by Turing, who demonstrated that a system of reacting and diffusing chemicals, called morphogens, can interact so as to produce stable nonuniform concentration patterns in space. Recently, a Turing model has been suggested to explain the development of pigmentation patterns on species of growing angelfish such as Pomacanthus semicirculatus, which exhibit readily observed changes in the number, size, and orientation of colored stripes during development of juvenile and adult stages, but the model fails to predict key features of the observations on stripe formation. Here we develop a generalized Turing model incorporating cell growth and movement, we analyze the effects of these processes on patterning, and we demonstrate that the model can explain important features of pattern formation in a growing system such as Pomacanthus. The applicability of classical Turing models to biological pattern formation is limited by virtue of the sensitivity of patterns to model parameters, but here we show that the incorporation of growth results in robustly generated patterns without strict parameter control. In the model, chemotaxis in response to gradients in a morphogen distribution leads to aggregation of one type of pigment cell into a striped spatial pattern.The coupling between growth and patterning, which is important in many developing systems (1-3), is particularly evident in the coloration patterns of the angelfish Pomacanthus (Fig. 1). Young angelfish of this genus display three vertical white stripes on a dark blue/black background, and as the fish grows, new stripes develop via gradual insertion between the preexisting stripes. This process repeats twice before the pattern undergoes a further transformation into its adult form. The first workers to suggest a mechanistic explanation for stripe doublings were Kondo and Asai (4), who proposed a Turing model (5) that predicts regular doubling of the number of morphogen peaks on a growing one-dimensional domain. Although their predictions are qualitatively consistent with the patterning sequence in the angelfish, there are several important observations that are not explained (6). In vivo, new stripes emerge gradually between preexisting stripes, first appearing faint and narrow, and then slowly widening, and the mature stripes are narrow in comparison with the region separating them. In contrast, the Kondo-Asai model predicts that the width of new stripes is nearly equal to that of mature stripes, and narrow stripes can only be obtained by choosing a threshold close to the peak of morphogen concentration, in which case stripe formation is unlikely to be robust to parameter variations. Furthermore, it is not known whether the one-dimensional peak doublings translate to two-dimensional stripe doublings. A Turing model on a geometrically realistic two-dimensional domain has been considered (7), but this model contains boundary sources that orient the pattern, in the absence of which only spo...

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“…the inner ear (reviewed in Erickson, 1993). EmbryologMelanocytes are found distributed in several organs, ically, melanocytes share with sensory and sympathetic such as the epidermis, the leptomeninges, the eye, and neurons a neural crest progenitor (reviewed in Holbrook et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Terminal differentiation and senescence in the human melanocyte: repression of tyrosine-phosphorylation of the extracellular signal-regulated kinase 2 selectively defines the two phenotypes.

Medrano

Yang

Boissy

et al. 1994

MBoC

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Melanocytes are pigmented cells distributed in humans in several organs like the epidermis, the leptomeninges, the eye, and the inner ear. Epidermal melanocytes, whether derived from adult or neonatal skin, proliferate well in a medium supplemented with phorbol esters and other mitogens before they undergo senescence. Potent cAMP inducers like cholera toxin are also growth promoters for neonatal melanocytes but only transient growth stimulators for cells derived from adults. We used this cellular system to delineate biochemical pathways involved in proliferation and in terminal differentiation. Here we show that after a period of 4-8 wk of sustained proliferation in the presence of cholera toxin, the adult melanocytes became round, flat, and enlarged. These changes were associated with terminal growth and preceded by a five-to sixfold increase in cAMP levels and an 8-to 10-fold increase in melanin content. The simultaneous addition of phorbol esters and cholera toxin did not prevent cells from reaching terminal differentiation. Identified targets for phorbol esters are protein kinase C (PKC) and the mitogen-activated kinases (MAPKs), also called extracellular signal-regulated kinases (ERKs). PKC was found to be similarly regulated in proliferating and in terminally differentiated melanocytes. Proliferating melanocytes in early or late passage showed identical activation of the kinase ERK2. This kinase was rapidly phosphorylated upon phorbol 12-myristate 13-acetate (PMA) addition and specifically accumulated in the nucleus of the cells, whereas in unstimulated cells it had a perinuclear distribution. In contrast, senescent and terminally differentiated cells were unable to phosphorylate tyrosine residues of the ERK2 gene product in spite of presenting normal amounts of ERK2 protein. In addition, ERK2 did not show the nuclear accumulation observed in proliferating melanocytes after PMA activation and remained localized in the perinuclear area. These results demonstrate that senescent and terminally differentiated melanocytes share a common block in a critical pathway thought to integrate multiple intracellular signals transmitted by various second messengers and specifically prevent the continuation of the signal transduction cascade initiated by PMA activation of PKC. (Lorton and Nordlund, 1991;Tassabehji et al., 1992;Urabe et al., 1993). When humans reach their fourth or fifth decade of life, the number of melanocytes in the epidermis, hair bulbs, eyes, and mucus membranes and the number of oral and cutaneous nevi begin to decrease (Nordlund, 1986). At the same time, there is a significant increase in the incidence of skin cancers. It is not known if the decrease in melanocyte numbers as humans age is because of premature senescence, terminal differentiation, or both phenomena. Possibly one result of the loss of melanocytes is a permissive environment for the development of malignancies. The possibility to grow human melanocytes in vitro to study the cellular and molecular mechanisms involved in melanocyte mig...

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From the Crest to the Periphery: Control of Pigment Cell Migration and Lineage Segregation

Cited by 73 publications

References 114 publications

Differential Gene Expression of TRPM1, the Potential Cause of Congenital Stationary Night Blindness and Coat Spotting Patterns (LP) in the Appaloosa Horse (Equus caballus)

Differential Gene Expression of TRPM1, the Potential Cause of Congenital Stationary Night Blindness and Coat Spotting Patterns (LP) in the Appaloosa Horse (Equus caballus)

Stripe formation in juvenile Pomacanthus explained by a generalized Turing mechanism with chemotaxis

Terminal differentiation and senescence in the human melanocyte: repression of tyrosine-phosphorylation of the extracellular signal-regulated kinase 2 selectively defines the two phenotypes.

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