Timing in the regulation of neural crest cell migration: Retarded “maturation” of regional extracellular matrix inhibits pigment cell migration in embryos of the white axolotl mutant

Löfberg, Jan; Perris, Roberto; Epperlein, Hans‐Henning

doi:10.1016/s0012-1606(89)80048-x

Cited by 53 publications

(26 citation statements)

References 31 publications

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“…The defect that produces this inhibition of migration may be associated with the extracellular matrix in the subepidermal space (Lofberg et al, 1989;Penis et al, 19901, and biochemical and histochemical characterization of this matrix shows that chondmitin and chondmitin-6-sulfate-rich proteoglycans are prominent in the white mutant ECM but are missing from the normal dark embryos . Although there may be other qualitative and quantitative differences in the subepiderma1 extracellular matrix between the white and dark embryos, these studies add to the growing evidence that some form of chondroitin sulfate regulates the timing of pigment cell migration in many different species.…”

Section: Patterns Of Migration Of Pigment Cellsmentioning

confidence: 99%

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

Erickson

1993

Pigment Cell Research

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Pigment cells are one of many cell types derived from the neural crest. This review focuses on the mechanisms that control the timing and pathways of migration of pigment cells into the epidermis and determinants that control the differentiation of pigment cells. Several factors may control the timing and pattern of pigment cell migration in the dorsolateral space including the loss of inhibitory molecules in the pathway, the appearance of chemotactic molecules emanating from the dispersing dermatome, and the differentiation of pigment cells, which may be the only neural crest derivative capable of utilizing the substratum found in the dorsolateral path.Control of pigment cell differentiation remains controversial. A working model presented in this review suggests that multipotent neural crest cells that disperse ventrally upon separation from the neural tube preserve neurogenic ability and lose melanogenic ability, whereas those cells that are arrested at the entrance to the dorsolateral path lose neurogenic ability so that the population becomes primarily melanogenic. During the time that the latter population is arrested in migration it is speculated that the neural crest cells are exposed to an environment comprised of specific extracellular matrix molecules and/or growth factors that enhance pigment cell differentiation.

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Section: Patterns Of Migration Of Pigment Cellsmentioning

confidence: 99%

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

Erickson

1993

Pigment Cell Research

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“…Later, the frequency of protrusion collapse decreases, allowing migration over the somite. Similarly, lateral pathway 'maturation' is indicated by heterologous extracellular matrix (ECM) transplantation studies in axolotl, with precocious NC migration initiated by ECM from older embryos (Löfberg et al, 1985;Löfberg et al, 1989). Two signals controlling the time when migration begins have been identified.…”

Section: Introductionmentioning

confidence: 99%

Sdf1a patterns zebrafish melanophores and links the somite and melanophore pattern defects inchokermutants

et al. 2007

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Pigment pattern formation in zebrafish presents a tractable model system for studying the morphogenesis of neural crest derivatives. Embryos mutant for choker manifest a unique pigment pattern phenotype that combines a loss of lateral stripe melanophores with an ectopic melanophore 'collar' at the head-trunk border. We find that defects in neural crest migration are largely restricted to the lateral migration pathway, affecting both xanthophores (lost) and melanophores (gained) in choker mutants. Double mutant and timelapse analyses demonstrate that these defects are likely to be driven independently, the collar being formed by invasion of melanophores from the dorsal and ventral stripes. Using tissue transplantation, we show that melanophore patterning depends upon the underlying somitic cells, the myotomal derivatives of which -both slow-and fast-twitch muscle fibres -are themselves significantly disorganised in the region of the ectopic collar. In addition, we uncover an aberrant pattern of expression of the gene encoding the chemokine Sdf1a in choker mutant homozygotes that correlates with each aspect of the melanophore pattern defect. Using morpholino knock-down and ectopic expression experiments, we provide evidence to suggest that Sdf1a drives melanophore invasion in the choker mutant collar and normally plays an essential role in patterning the lateral stripe. We thus identify Sdf1 as a key molecule in pigment pattern formation, adding to the growing inventory of its roles in embryonic development.

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“…A restricted access of primary antibodies due to a relative epitope clustering could account for the lower immunoreactivity of IMPG. 5 When epidermal explants were simultaneously labeled with axolotl embryo, PGs appear to be localized along collagen fibrils, seemingly attached to them (27)(28)(29)(30). Moreover, chicken PG-M has been shown to be able to bind to type I collagen (39).…”

Section: Discussionmentioning

confidence: 99%

PG-M/Versican-like Proteoglycans Are Components of Large Disulfide-stabilized Complexes in the Axolotl Embryo

Stigson

Löfberg

Kjellén

1997

Journal of Biological Chemistry

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Large disulfide-stabilized proteoglycan complexes were previously shown to be synthesized by the epidermis of axolotl embryos during stages crucial to subepidermal migration of neural crest cells. We now show that the complexes contain PG-M/versican-like monomers in addition to some other component with low buoyant density. Metabolically 35 S-labeled proteoglycans were extracted from epidermal explants and separated by size exclusion chromatography and density equilibrium gradient centrifugation. The complexes, which elute in the void volume on Sepharose CL-2B, were recovered at buoyant density 1.42 g/ml in CsCl gradients, whereas the monomer proteoglycans, which could only be liberated from the complexes by reduction, had a higher buoyant density (1.48 g/ml). The native complexes did not aggregate with hyaluronan. The purified complexes reacted with antibodies against a portion of a cloned PG-M/versican-like axolotl proteoglycan. These antibodies were found to stain the subepidermal matrix of axolotl embryos, suggesting that the proteoglycan complexes are encountered by neural crest cells during subepidermal migration. From Western blot analysis, the core protein of the PG-M/versicanlike monomers was found to be of similar size (Ϸ500 kDa) as those of PG-M/versican variants of other species. Another chondroitin sulfate proteoglycan that was present in small amounts in the epidermal extracts was found to be distinctly different from the similarly sized PG-M/versican-like monomers.The role of proteoglycans (PGs) 1 in the modulation of cellmatrix interaction and cell migration depends on their structure and localization (1-3). Interstitial PGs that carry chondroitin/dermatan sulfate (CS/DS) chains have been implicated to have such modulatory roles by several studies (4 -18). In this regard, since both the core protein (7, 18 -19) and the glycosaminoglycan moiety (15,18,20) appear to be of functional importance, the structure of the intact PG may be crucial (9,18). In addition to the inherent potential for heterogeneity in the carbohydrate component (21), the core proteins of PGs in the PG-M/versican family, for instance, may exist as several splice variants (22-25) with potentially diverse expression patterns and functions during various stages of the life cycle of an animal.The importance of the extracellular matrix in the regulation of subepidermal neural crest cell migration in the axolotl embryo was demonstrated by transplantation experiments in which epidermal grafts or microcarriers with matrix adsorbed in situ from developmentally more advanced embryos were found to trigger the onset of premature migration (26). Ultrastructural studies of the matrix after fixation in the presence of cetylpyridinium chloride (27) or ruthenium red (28 -30) revealed an abundance of granular proteoglycan precipitates along collagen fibrils. Interestingly, in embryos of the white mutant axolotl, in which subepidermal migration of the neural crest-derived pigment cells is defective (28 -29, 31), the subepidermal matrix was sign...

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Timing in the regulation of neural crest cell migration: Retarded “maturation” of regional extracellular matrix inhibits pigment cell migration in embryos of the white axolotl mutant

Cited by 53 publications

References 31 publications

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

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

Sdf1a patterns zebrafish melanophores and links the somite and melanophore pattern defects inchokermutants

PG-M/Versican-like Proteoglycans Are Components of Large Disulfide-stabilized Complexes in the Axolotl Embryo

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