Spatiotemporal changes in HNK-1/L2 glycoconjugates on avian embryo somite and neural crest cells

Newgreen, Donald F.; Powell, M. E. A.; Moser, Berthold

doi:10.1016/0012-1606(90)90282-n

Cited by 74 publications

(55 citation statements)

References 63 publications

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“…There is considerable evidence that sclerotome plays a role in regulating neural crest migration in avian and mammalian embryos (Bronner-Fraser, 1986;Loring and Erickson, 1987;Teillet et al, 1987;Newgreen et al, 1990); however, the role of myotome in initial patterning of neural crest migration has received less attention. Many studies document neural crest migration on the anterior halfsclerotome of each somite, and several molecules expressed in posterior half-sclerotome have been shown to repel neural crest migration (Newgreen et al, 1990) (reviewed by Le Douarin and Kalcheim, 1999;Krull, 2001;Kalcheim, 2000). However, Tosney et al (Tosney et al, 1994) provided evidence that neural crest cells prefer to migrate on the myotome basal lamina rather than on sclerotome.…”

Section: Discussionmentioning

confidence: 99%

“…Although many studies in amniote embryos have implicated sclerotome in patterning neural crest migration (Newgreen et al, 1990) (reviewed by Le Douarin and Kalcheim, 1999;Krull, 2001;Kalcheim, 2000), in zebrafish, neural crest cells do not encounter sclerotome cells until the segmental pattern of neural crest migration streams is already established (Morin-Kensicki and Eisen, 1997). Thus, it is unlikely that sclerotome participates in the initial patterning of neural crest migration, although we cannot rule out a role of sclerotome in later stages of neural crest migration, particularly migration ventral of the horizontal myoseptum.…”

Section: Fast Muscle Cells Are Not Required For Formation Of Normal Nmentioning

confidence: 99%

“…In avian and mammalian embryos, trunk neural crest migration is regulated by environmental cues thought to be derived from somites, and especially from sclerotome. Many studies provide evidence that neural crest migrates through the anterior half sclerotome of each somite, and several molecules expressed in posterior half sclerotome repel crest migration (Newgreen et al, 1990) (reviewed by Le Douarin and Kalcheim, 1999;Krull, 2001;Kalcheim, 2000;Kuan et al, 2004). In contrast to amniote embryos, the majority of cells in the somites of anamniotes such as zebrafish and frogs are myotomal, rather than sclerotomal ( Fig.…”

Section: Introductionmentioning

confidence: 99%

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Slow muscle regulates the pattern of trunk neural crest migration in zebrafish

Honjo

Eisen

2005

Development

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In avians and mice, trunk neural crest migration is restricted to the anterior half of each somite. Sclerotome has been shown to play an essential role in this restriction; the potential role of other somite components in specifying neural crest migration is currently unclear. By contrast, in zebrafish trunk neural crest, migration on the medial pathway is restricted to the middle of the medial surface of each somite. Sclerotome comprises only a minor part of zebrafish somites, and the pattern of neural crest migration is established before crest cells contact sclerotome cells, suggesting other somite components regulate the pattern of zebrafish neural crest migration. Here, we use mutants to investigate which components regulate the pattern of zebrafish trunk neural crest migration on the medial pathway. The pattern of trunk neural crest migration is aberrant in spadetail mutants that have very reduced somitic mesoderm, in no tail mutants injected with spadetail morpholino antisense oligonucleotides that entirely lack somitic mesoderm and in somite segmentation mutants that have normal somite components but disrupted segment borders. Fast muscle cells appear dispensable for patterning trunk neural crest migration. However, migration is abnormal in Hedgehog signaling mutants that lack slow muscle cells, providing evidence that slow muscle cells regulate the pattern of trunk neural crest migration. Consistent with this idea, surgical removal of adaxial cells, which are slow muscle precursors, results in abnormal patterning of neural crest migration;normal patterning can be restored by replacing the ablated adaxial cells with ones transplanted from wild-type embryos.

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Section: Discussionmentioning

confidence: 99%

Section: Fast Muscle Cells Are Not Required For Formation Of Normal Nmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Slow muscle regulates the pattern of trunk neural crest migration in zebrafish

Honjo

Eisen

2005

Development

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“…Similarly, macromolecules isolated from posterior somite halves using a PNA-affinity column cause the collapse of motor neuron growth cones (Davies et al, 1990). Moreover, the presence of chondroitin sulfate proteoglycan and PNAbinding activity is associated with other tissues through which the neural crest cells do not invade, such as the posterior somite and the perinotochordal space l l n et al, 1987;Newgreen et al, 1990;Tosney and Oakley, 1990;Perris et al, 1991b).…”

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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“…It is widely accepted that during development, the HNK1 epitope is expressed in migrating neural crest cells as well as in other tissues (Bannerman et al, 1998;Luider et al, 1993;Newgreen et al, 1990;Tucker et al, 1984;Vincent and Thiery 1984). Studies of cardiogenesis have revealed that the HNK1 epitope is expressed on the cell surface of the developing conduction myocardium in a variety of species (Aoyama et al, 1995;Chuck and Watanabe 1997;Gorza et al, 1988;Ikeda et al, 1990;Nakagawa et al, 1993).…”

mentioning

confidence: 99%

Expression of HNK1 epitope by the cardiomyocytes of the early embryonic chick: In situ and in vitro studies

et al. 2001

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Monoclonal antibody HNK1 reacts with a carbohydrate epitope in cell surface glycoproteins and glycolipids. During development, in various species the HNK1 epitopes are expressed in migrating neural crest cells and in the developing conduction cardiomyocytes. The conduction system is generally thought to be developed from cardiomyocytes, but some investigators have hypothesized that it is derived from the neural crest because conduction myocytes express neural antigens, including HNK1. Using immunohistochemistry, we examined the spatiotemporal expression of HNK1 in early chick cardiogenesis (stages 4 to 18) and whether cultured precardiac mesoderm does or does not express HNK1 as well as sarcomeric myosin (MF20). HNK1 was first expressed in the premyocardium at stage 8. At stage 10, HNK1-positive cardiomyocytes were scattered along the straight heart tube. By stage 18, HNK1-positive cardiomyocytes had become restricted to the atrium and sinus venosus. Atrioventricular cushion mesenchyme also expressed an HNK1 epitope. Immunostaining of HNK1 and MF20 in cultured precardiac mesoderm showed that there are at least three types of cells: 1) cardiomyocytes without HNK1 expression, 2) cells possessing both HNK1-and MF20-immunoreactivity, and 3) mesenchymal cells with HNK1. Immunogold electron microscopy showed that cardiomyocytes containing sparsely distributed myofibrils associated with the Z-band react with anti-HNK1 antibody. Our observations showed a direct evidence for the first time that the precardiac mesoderm generates HNK1-positive cardiomyocytes with morphological features similar to those of conduction cardiomyocytes.

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Spatiotemporal changes in HNK-1/L2 glycoconjugates on avian embryo somite and neural crest cells

Cited by 74 publications

References 63 publications

Slow muscle regulates the pattern of trunk neural crest migration in zebrafish

Slow muscle regulates the pattern of trunk neural crest migration in zebrafish

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

Expression of HNK1 epitope by the cardiomyocytes of the early embryonic chick: In situ and in vitro studies

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