Clonal analysis of quail neural crest cells: they are pluripotent and differentiate in vitro in the absence of non-crest cells. Dev Biol
ABSTRACT To determine if neural crest cells are pluripotent and establish whether differentiation occurs in the absence of noncrest cells, a cell culture method was devised in which differentiation could be examined in clones derived from single, isolated neural crest cells. Single neural crest cells, which were isolated before the onset of in vivo migration, gave rise to three types of clones: pigmented, unpigmented, and mixed. Pigmented clones consisted of melanocytes only, whereas some unpigmented cells in mixed and unpigmented clones contained catecholamines, identifying them as adrenergic cells. Extracellular matrix derived from quail somite or chick skin fibroblast cultures stimulated adrenergic differentiation and axon formation. These results demonstrate for the first time the existence of pluripotent quail neural crest cells that give rise to at least two progeny, melanocytes and neuronal cells. They also suggest that continuous direct interactions with noncrest cells are not required for the differentiation of these two cell types. However, components of the extracellular matrix derived from noncrest cells may play an important role in expression of the adrenergic phenotype.
- SourceAvailable from: Carla Real
- "Given the diversity of the derivatives generated by the NC in vivo, several attempts aimed at elucidating how and when the different NC-lineages become segregated during ontogeny, have been made by testing the developmental potential of individual NC cells in vitro and in vivo. Seminal experiments of in vitro clonal assays performed three decades ago by Cohen and collaborators unravelled that avian trunk NC cells migrating from cultured neural tubes are heterogeneous with respect to their potential to give rise to unpigmented and pigmented progeny  . The sound evidence for multipotency of NC cells in vivo was put forward by lineage tracing of the progeny of individual cells labelled following microinjection of vital fluorescent dye in the avian embryo  . "
Dataset: dupin 2007
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- "types, including osteocytes, chondrocytes, and sensory neurons. Cell labeling studies indicate that neural crest cells are initially multipotent but gradually become lineagerestricted in developmental potential (Dorsky et al., 1998; Sieber-Blum and Cohen, 1980). "
ABSTRACT: Melanocytes are pigment-producing cells in the skin of humans and other vertebrates. A number of genes involved in melanocyte development and vertebrate pigmentation have been characterized, largely through studies of a diversity of pigment mutations in a variety of species. Embryonic development of the melanocyte initiates with cell fate specification in the neural crest, which is then followed by cell migration and niche localization. Many genes involved in melanocyte development have also been implicated in the development of melanoma, an aggressive and fatal form of skin cancer that originates in the melanocyte. Although early stage melanomas that have not spread to the lymph nodes can be excised with little risk of recurrence, patients diagnosed with metastatic melanoma have a high mortality rate due to the resistance of most tumors to radiotherapy and chemotherapy. Transformed melanocytes that develop into melanomas proliferate abnormally and often begin to grow radially in the skin. Vertical growth can then follow this radial growth, leading to an invasion through the basement membrane into the underlying dermis and subsequent metastasis. It is still unclear, however, how a normal melanocyte becomes a melanoma cell, and how melanoma utilizes the properties of the normal melanocyte and its progenitors in its progression. The goal of this mini-review is to highlight the role of melanocyte developmental pathways in melanoma, and to discuss recent studies and tools being used to illuminate this connection.Journal of Cellular Physiology 01/2010; 222(1):38-41. DOI:10.1002/jcp.21935 · 3.87 Impact Factor
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- "In vitro studies have followed the progeny of single NC cells in clones (Le Douarin and Kalcheim, 1999). Some studies find a very heterogeneous mixture of clones, including some with many different NC cell types, and have been interpreted to support the existence of multipotential NC cells that become progressively fate restricted (Dupin et al., 1998; Sieber-Blum and Cohen, 1980; Stemple and Anderson, 1992). Other studies find that almost half the clones are of a single phenotype and support an argument for distinct NC lineages that diverge before or soon after crest cells emerge from the neural tube (Henion and Weston, 1997; Luo et al., 2003). "
ABSTRACT: Neural crest (NC) cells arise in the dorsal neural tube (NT) and migrate into the embryo to develop into many different cell types. A major unresolved question is when and how the fate of NC cells is decided. There is widespread evidence for multipotential NC cells, whose fates are decided during or after migration. There is also some evidence that the NC is already divided into subpopulations of discrete precursors within the NT. We have investigated this question in the mouse embryo. We find that a subpopulation of cells on the most dorsomedial aspect of the NT express the receptor tyrosine kinase Kit (previously known as c-kit), emigrate exclusively into the developing dermis, and then express definitive markers of the melanocyte lineage. These are thus melanocyte progenitor cells. They are generated predominantly at the midbrain-hindbrain junction and cervical trunk, with significant numbers also in lower trunk. Other cells within the dorsal NT are Kit-, migrate ventrally, and, from embryonic day 9.5, express the neurotrophin receptor p75. These cells most likely only give rise to ventral NC derivatives such as neurons and glia. The p75+ cells are located ventrolateral to the Kit+ cells in areas of the NT where these two cell types are found. These data provide direct in vivo evidence for NC lineage segregation within the mouse neural tube.Development 01/2005; 131(24):6153-62. DOI:10.1242/dev.01533 · 6.27 Impact Factor