Neural crest cells regulate optic cup morphogenesis by promoting extracellular matrix assembly

2018 ◽  
Author(s):  
Ashrifia Adomako-Ankomah
Keyword(s):  
Extracellular Matrix ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Matrix Assembly ◽  
Optic Cup

scholarly journals Neural crest cells regulate optic cup morphogenesis by promoting extracellular matrix assembly

2018 ◽  
Author(s):  
Chase D. Bryan ◽  
Rebecca L. Pfeiffer ◽  
Bryan W. Jones ◽  
Kristen M. Kwan
Keyword(s):  
Extracellular Matrix ◽  
Neural Crest ◽  
Cell Tracking ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Neural Crest Cells ◽  
Underlying Mechanism ◽  
Ultrastructural Level ◽  
Matrix Assembly ◽  
Optic Cup

AbstractThe interactions between an organ and its surrounding environment are critical in regulating its development. In vertebrates, neural crest and mesodermal mesenchymal cells have been observed close to the eye during development, and mutations affecting this periocular mesenchyme can cause defects in early eye development, yet the underlying mechanism has been unknown. Here, using timelapse microscopy and four-dimensional cell tracking in zebrafish, we establish that genetic loss of neural crest impairs cell movements within the optic vesicle. At the ultrastructural level, neural crest cells are required for basement membrane formation specifically around the retinal pigment epithelium. Neural crest cells express the extracellular matrix crosslinking protein nidogen and, strikingly, ectopically expressing nidogen in the absence of neural crest partially restores optic cup morphogenesis. These results demonstrate that the neural crest is required for local establishment of ocular extracellular matrix superstructure, which in turn drives optic cup morphogenesis.

The role of cell-extracellular matrix interactions in neural crest cell migration

1989 ◽  
Vol 47 ◽  
pp. 842-843
Author(s):  
Marianne Bronner-Fraser
Keyword(s):  
Extracellular Matrix ◽  
Cell Migration ◽  
Neural Crest ◽  
Cell Movement ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Pigment Cells ◽  
Surrounding Matrix ◽  
Adrenal Chromaffin ◽  
Crest Cell

The formation of the embryo involves intricate cell movements, cell proliferation, and differentiation. The neural crest has long served as a model for the study of these processes because these cells: 1. migrate extensively along characteristic pathways during embryogenesis. 2. give rise to diverse and numerous derivatives, including pigment cells, adrenal chromaffin cells, and the ganglia of the peripheral nervous system; and 3. are accessible to surgical, immunological, and biochemical manipulations during both initial and certain later stages in their development. We are in the process of identifying factors that influence cell migration and differentiation in the neural crest system.Neural crest cells follow two primary migratory pathways in the trunk: a dorsolateral route underneath the skin, and a ventral route through the somite. Within the somites, neural crest cells preferentially migrate through the rostral half of each sclerotome but are absent from the caudal sclerotome. The regions through which neural crest cells migrate are lined with extracellular matrix (ECM) molecules. Because of the intimate relationship between neural crest cells and the surrounding matrix, it has been proposed that the ECM plays an important role in the initiation, guidance, and cessation of neural crest cell movement.

scholarly journals Mitf-family transcription factor function is required within cranial neural crest cells to promote choroid fissure closure

2019 ◽  
Author(s):  
Katie L. Sinagoga ◽  
Alessandra M. Larimer-Picciani ◽  
Stephanie M. George ◽  
Samantha A. Spencer ◽  
James A. Lister ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Cranial Neural Crest ◽  
Cellular Mechanisms ◽  
Optic Cup ◽  
Summary Statement ◽  
Cranial Neural Crest Cells ◽  
And Function ◽  
Choroid Fissure

AbstractA critical step in eye development is closure of the choroid fissure (CF), a transient structure in the ventral optic cup through which vasculature enters the eye and ganglion cell axons exit. While many factors have been identified that function during CF closure, the molecular and cellular mechanisms mediating this process remain poorly understood. Failure of CF closure results in colobomas. Recently, MITF was shown to be mutated in a subset of human coloboma patients, but how MITF functions during CF closure is unknown. To address this question, zebrafish with mutations in mitfa and tfec, two members of the Mitf-family of transcription factors, were analyzed and their functions during CF closure determined. mitfa;tfec mutants possess severe colobomas and our data demonstrate that Mitf activity is required within cranial neural crest cells (cNCCs) to facilitate CF closure. In the absence of Mitf function, cNCC migration and localization in the optic cup are perturbed. These data shed light on the cellular mechanisms underlying colobomas in patients with MITF mutations and identify a novel role for Mitf function in cNCCs during CF closure.Summary StatementMitf-family transcription factors act within cranial neural crest cells to promote choroid fissure closure. Without Mitf-family function, cNCC localization and function in the CF is disrupted, thus contributing to colobomas.

Extracellular matrix from normal but not Steel mutant mice enhances melanogenesis in cultured mouse neural crest cells

1990 ◽  
Vol 139 (2) ◽  
pp. 299-307 ◽  
Author(s):  
Kathleen Morrison-Graham ◽  
Lisa West-Johnsrud ◽  
James A. Weston
Keyword(s):  
Extracellular Matrix ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Mutant Mice
Sign in / Sign up

Export Citation Format

Share Document