Neural crest cell migratory pathways in the trunk of the chick embryo

Loring, Jeanne F.; Erickson, Carol A.

doi:10.1016/0012-1606(87)90154-0

Cited by 270 publications

(212 citation statements)

References 35 publications

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“…However, ventral migration is more intricately patterned than is generally thought, and the patterns accord with quite detailed spatialtemporal patterns of somite maturation (Fig. 6 summarizes results from Rickmann et al, 1985;BronnerFraser, 1986;Loring andErickson, 1987, Teillet et al, 1987;Tosney, 1987;Serbedzija et al, 1990;Tosney and Oakley, 1990;Bronner-Fraser and Stern, 1991;Oakley et al, 1994;Tosney et al, 1994;Hotary and Tosney, 1996;Sela-Donenfeld and Kalcheim, 2000). It remains unclear whether different ventral routes provide population-specific cues.…”

Section: Discussionmentioning

confidence: 55%

Long‐distance cue from emerging dermis stimulates neural crest melanoblast migration

Tosney

2003

Developmental Dynamics

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Neural crest melanoblasts display unique navigational abilities enabling them to colonize the dorsal path between ectoderm and somite. One signal shown here to elicit melanoblast migration is a chemotactic cue supplied by the emerging dermis. Until dermis emerges, melanoblasts fail to enter the dorsal path. The dermis emerges from a site that is too distant to stimulate migration by cell contact. Instead, surgeries show that dermis elicits migration from a distance. When dermis is grafted distally, neural crest cells enter the path precociously. Moreover, large grafts recruit melanoblasts from the control sides (without increasing crest cell numbers) as well as a few crest cells from ventral somite. Because other grafted tissues fail to stimulate migration, the dermis stimulus is specific. This report is the first documentation that trunk neural crest cells can be guided chemotactically. It also extends evidence that migration is exquisitely sensitive to temporal-spatial patterns of somite morphogenesis. Developmental Dynamics 229:99 -108, 2004.

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Section: Discussionmentioning

confidence: 55%

Long‐distance cue from emerging dermis stimulates neural crest melanoblast migration

Tosney

2003

Developmental Dynamics

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“…3 C-E). It is interesting that tumor cells populated ventral sites typical of neuronal NCC precursors rather than following dorsolateral migratory pathways thought to be linked to NCCs that become melanocytes (28). There is an ongoing debate in the NCC literature as to when trunk NCCs truly adopt a particular cell fate (29).…”

Section: Discussionmentioning

confidence: 99%

Reprogramming metastatic melanoma cells to assume a neural crest cell-like phenotype in an embryonic microenvironment

Kulesa

Kasemeier-Kulesa

Teddy

et al. 2006

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

227

218

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Human metastatic melanoma cells express a dedifferentiated, plastic phenotype, which may serve as a selective advantage, because melanoma cells invade various microenvironments. Over the last three decades, there has been an increased focus on the role of the tumor microenvironment in cancer progression, with the goal of reversing the metastatic phenotype. Here, using an embryonic chick model, we explore the possibility of reverting the metastatic melanoma phenotype to its cell type of origin, the neural-crest-derived melanocyte. GFP-labeled adult human metastatic melanoma cells were transplanted in ovo adjacent to host chick premigratory neural crest cells and analyzed 48 and 96 h after egg reincubation. Interestingly, the transplanted melanoma cells do not form tumors. Instead, we find that transplanted melanoma cells invade surrounding chick tissues in a programmed manner, distributing along host neural-crest-cell migratory pathways. The invading melanoma cells display neural-crest-cell-like morphologies and populate host peripheral structures, including the branchial arches, dorsal root and sympathetic ganglia. Analysis of a melanocyte-specific phenotype marker (MART-1) and a neuronal marker (Tuj1) revealed a subpopulation of melanoma cells that invade the chick periphery and express MART-1 and Tuj1. Our results demonstrate the ability of adult human metastatic melanoma cells to respond to chick embryonic environmental cues, a subset of which may undergo a reprogramming of their metastatic phenotype. This model has the potential to provide insights into the regulation of tumor cell plasticity by an embryonic milieu, which may hold significant therapeutic promise.plasticity ͉ chick ͉ MART-1 ͉ epigenetic

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“…The adrenal cortex develops from mesoderm and produces mineralocorticoid and glucocorticoid hormones, whereas the adrenal medulla consists of neural crest-derived chromaffin cells and releases the catecholamines adrenaline and noradrenaline. To form the adrenal medulla, trunk neural crest cells that belong to the sympathoadrenal sublineage have to migrate from the dorsal aspect of the neural tube through the anterior part of the somites and past the dorsal aorta to the adrenal anlage (Loring and Erickson, 1987). At the dorsal aorta, neural crest cells are instructed by bone morphogenetic protein (BMP) signals to develop into catecholaminergic precursors, which are marked by expression of a set of transcription factors, including paired homeobox 2b (Phox2b), mammalian achaete scute homolog 1 (Mash1), Gata3, and Hand2 (for a recent review, see Goridis and Rohrer, 2002;Huber, 2006).…”

Section: Introductionmentioning

confidence: 99%

SoxE Proteins Are Differentially Required in Mouse Adrenal Gland Development

Reiprich

Stolt

Schreiner

et al. 2008

MBoC

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Sry-box (Sox)8, Sox9, and Sox10 are all strongly expressed in the neural crest. Here, we studied the influence of these closely related transcription factors on the developing adrenal medulla as one prominent neural crest derivative. Whereas Sox9 was not expressed, both Sox8 and Sox10 occurred widely in neural crest cells migrating to the adrenal gland and in the gland itself, and they were down-regulated in cells expressing catecholaminergic traits. Sox10-deficient mice lacked an adrenal medulla. The adrenal anlage was never colonized by neural crest cells, which failed to specify properly at the dorsal aorta and died apoptotically during migration. Furthermore, mutant neural crest cells did not express Sox8. Strong adrenal phenotypes were also observed when the Sox10 dimerization domain was inactivated or when a transactivation domain in the central portion was deleted. Sox8 in contrast had only minimal influence on adrenal gland development. Phenotypic consequences became only visible in Sox8-deficient mice upon additional deletion of one Sox10 allele. Replacement of Sox10 by Sox8, however, led to significant rescue of the adrenal medulla, indicating that functional differences between the two related Sox proteins contribute less to the different adrenal phenotypes of the null mutants than dependence of Sox8 expression on Sox10.

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Neural crest cell migratory pathways in the trunk of the chick embryo

Cited by 270 publications

References 35 publications

Long‐distance cue from emerging dermis stimulates neural crest melanoblast migration

Long‐distance cue from emerging dermis stimulates neural crest melanoblast migration

Reprogramming metastatic melanoma cells to assume a neural crest cell-like phenotype in an embryonic microenvironment

SoxE Proteins Are Differentially Required in Mouse Adrenal Gland Development

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