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Biomedical subjects

Laura S Gammill

Publications and source records attributed to Laura S Gammill.

6 recordsLinked to original sources
PubMed2005

Guidance of trunk neural crest migration requires neuropilin 2/semaphorin 3F signaling.

In vertebrate embryos, neural crest cells migrate only through the anterior half of each somite while avoiding the posterior half. We demonstrate that neural crest cells express the receptor neuropilin 2 (Npn2), while its repulsive ligand semaphorin 3F (Sema3f) is restricted to the posterior-half somite. In Npn2 and Sema3f mutant mice, neural crest cells lose their segmental migration pattern and instead migrate as a uniform sheet, although somite polarity itself remains unchanged. Furthermore, Npn2 is cell autonomously required for neural crest cells to avoid Sema3f in vitro. These data show that Npn2/Sema3f signaling guides neural crest migration through the somite. Interestingly, neural crest cells still condense into segmentally arranged dorsal root ganglia in Npn2 nulls, suggesting that segmental neural crest migration and segmentation of the peripheral nervous system are separable processes.

Animals↗
PubMed2005

Abnormalities in neural crest cell migration in laminin alpha5 mutant mice.

Although numerous in vitro experiments suggest that extracellular matrix molecules like laminin can influence neural crest migration, little is known about their function in the embryo. Here, we show that laminin alpha5, a gene up-regulated during neural crest induction, is localized in regions of newly formed cranial and trunk neural folds and adjacent neural crest migratory pathways in a manner largely conserved between chick and mouse. In laminin alpha5 mutant mice, neural crest migratory streams appear expanded in width compared to wild type. Conversely, neural folds exposed to laminin alpha5 in vitro show a reduction by half in the number of migratory neural crest cells. During gangliogenesis, laminin alpha5 mutants exhibit defects in condensing cranial sensory and trunk sympathetic ganglia. However, ganglia apparently recover at later stages. These data suggest that the laminin alpha5 subunit functions as a cue that restricts neural crest cells, focusing their migratory pathways and condensation into ganglia. Thus, it is required for proper migration and timely differentiation of some neural crest populations.

Animals↗
PubMed2005

Specification of the enveloping layer and lack of autoneuralization in zebrafish embryonic explants.

We have analyzed the roles of cell contact during determination of the outermost enveloping layer (EVL) and deeper neurectoderm in zebrafish embryos. Outer cells, but not deeper cells, are specified to express the EVL-specific marker, cyt1 by late blastula. EVL specification requires cell contact or close cell proximity, because cyt1 is not expressed after explant dissociation. The EVL may be homologous to the Xenopus epithelial layer, including the ventral larval epidermis. While Xenopus epidermal cytokeratin gene expression is activated by bone morphogenetic protein (BMP) signaling, zebrafish cyt1 is not responsive to BMPs. Zebrafish early gastrula ectodermal explants are specified to express the neural markers opl (zic1) and otx2, and this expression is prevented by BMP4. Dissociation of zebrafish explants prevents otx2 and opl expression, suggesting that neural specification in zebrafish requires cell contact or close cell proximity. This finding is in contrast to the case in Xenopus, where ectodermal dissociation leads to activation of neural gene expression, or autoneuralization. Our data suggest that distinct mechanisms direct development of homologous lineages in different vertebrates.

Amino Acid Sequence↗
PubMed2004

Discovery of genes implicated in placode formation.

The peripheral nervous system of the head is derived from cranial ectodermal placodes and neural crest cells. Placodes arise from thickenings in the cranial ectoderm that invaginate or ingress to form sensory ganglia and the paired sense organs. We have combined embryological techniques with array technology to identify genes that are expressed as a consequence of placode induction. As a secondary screen, we used whole mount in situ hybridization to determine the expression of candidate genes in various placodal domains. The results reveal 52 genes that are found in one or more placodes, including the olfactory, trigeminal, and otic placodes. Expression of some of these genes is retained in placodal derivatives. Furthermore, several genes are common to both neural crest and ectodermal placodes. This study presents the first array of candidate genes implicated in placode development, providing numerous new molecular markers for various stages of placode formation. Importantly, the results uncover previously unknown commonalities in genes expressed by multiple placodes and shared properties between placodes and other migratory cells, like neural crest cells.

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PubMed2002

Genomic analysis of neural crest induction.

The vertebrate neural crest is a migratory stem cell population that arises within the central nervous system. Here, we combine embryological techniques with array technology to describe 83 genes that provide the first gene expression profile of a newly induced neural crest cell. This profile contains numerous novel markers of neural crest precursors and reveals previously unrecognized similarities between neural crest cells and endothelial cells, another migratory cell population. We have performed a secondary screen using in situ hybridization that allows us to extract temporal information and reconstruct the progression of neural crest gene expression as these cells become different from their neighbors and migrate. Our results reveal a sequential 'migration activation' process that reflects stages in the transition to a migratory neural crest cell and suggests that migratory potential is established in a pool of cells from which a subset are activated to migrate.

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