scholarly journals KirrelL, a member of the Ig-domain superfamily of adhesion proteins, is essential for fusion of primary mesenchyme cells in the sea urchin embryo

2017 ◽  
Vol 421 (2) ◽  
pp. 258-270 ◽  
Author(s):  
Charles A. Ettensohn ◽  
Debleena Dey
Keyword(s):  
Sea Urchin ◽  
Adhesion Proteins ◽  
Sea Urchin Embryo ◽  
Mesenchyme Cells ◽  
Ig Domain ◽  
Primary Mesenchyme Cells

Localization and expression of msp130, a primary mesenchyme lineage-specific cell surface protein in the sea urchin embryo

Development ◽  
1987 ◽  
Vol 101 (2) ◽  
pp. 255-265 ◽  
Author(s):  
J.A. Anstrom ◽  
J.E. Chin ◽  
D.S. Leaf ◽  
A.L. Parks ◽  
R.A. Raff
Keyword(s):  
Cell Surface ◽  
Sea Urchin ◽  
Sea Water ◽  
Surface Protein ◽  
Specific Cell ◽  
Cell Surface Protein ◽  
Sea Urchin Embryo ◽  
A Cell ◽  
Mesenchyme Cells ◽  
Primary Mesenchyme Cells

In this report, we use a monoclonal antibody (B2C2) and antibodies against a fusion protein (Leaf et al. 1987) to characterize msp130, a cell surface protein specific to the primary mesenchyme cells of the sea urchin embryo. This protein first appears on the surface of these cells upon ingression into the blastocoel. Immunoelectronmicroscopy shows that msp130 is present in the trans side of the Golgi apparatus and on the extracellular surface of primary mesenchyme cells. Four precursor proteins to msp130 are identified and we show that B2C2 recognizes only the mature form of msp130. We demonstrate that msp130 contains N-linked carbohydrate groups and that the B2C2 epitope is sensitive to endoglycosidase F digestion. Evidence that msp130 is apparently a sulphated glycoprotein is presented. The recognition of the B2C2 epitope of msp130 is disrupted when embryos are cultured in sulphate-free sea water. In addition, two-dimensional immunoblots show that msp130 is an acidic protein that becomes substantially less acidic in the absence of sulphate. We also show that two other independently derived monoclonal antibodies, IG8 (McClay et al. 1983; McClay, Matranga & Wessel, 1985) and 1223 (Carson et al. 1985), recognize msp130, and suggest this protein to be a major cell surface antigen of primary mesenchyme cells.

scholarly journals Culture of and experiments with sea urchin embryo primary mesenchyme cells

2019 ◽  
pp. 293-330
Author(s):  
Bradley Moreno ◽  
Allessandra DiCorato ◽  
Alexander Park ◽  
Kellen Mobilia ◽  
Regina Knapp ◽  
...  
Keyword(s):  
Sea Urchin ◽  
Sea Urchin Embryo ◽  
Mesenchyme Cells ◽  
Primary Mesenchyme Cells

Pattern formation during gastrulation in the sea urchin embryo

Development ◽  
1992 ◽  
Vol 116 (Supplement) ◽  
pp. 33-41 ◽  
Author(s):  
David R. McClay ◽  
Norris A. Armstrong ◽  
Jeff Hardin
Keyword(s):  
Sea Urchin ◽  
Spatial Information ◽  
Cell Types ◽  
Cell Interactions ◽  
Pigment Cells ◽  
Original Position ◽  
Embryonic Cells ◽  
Sea Urchin Embryo ◽  
Mesenchyme Cells ◽  
Primary Mesenchyme Cells

The sea urchin embryo follows a relatively simple cell behavioral sequence in its gastrulation movements. To form the mesoderm, primary mesenchyme cells ingress from the vegetal plate and then migrate along the basal lamina lining the blastocoel. The presumptive secondary mesenchyme and endoderm then invaginate from the vegetal pole of the embryo. The archenteron elongates and extends across the blastocoel until the tip of the archenteron touches and attaches to the opposite side of the blastocoel. Secondary mesenchyme cells, originally at the tip of the archenteron, differentiate to form a variety of structures including coelomic pouches, esophageai muscles, pigment cells and other cell types. After migration of the secondary mesenchyme cells from their original position at the tip of the archenteron, the endoderm fuses with an invagination of the ventral ectoderm (the stomodaem), to form the mouth and complete the process of gastrulation. A larval skeleton is made by primary mesenchyme cells during the time of archenteron and mouth formation. A number of experiments have established that these morphogenetic movements involve a number of cell autonomous behaviors plus a series of cell interactions that provide spatial, temporal and scalar information to cells of the mesoderm and endoderm. The cell autonomous behaviors can be demonstrated by the ability of micromeres or endoderm to perform their morphogenetic functions if either is isolated and grown in culture. The requirement for cell interactions has been demonstrated by manipulative experiments where it has been shown that axial information, temporal information, spatial information and scalar information is obtained by mesoderm and endoderm from other embryonic cells. This information governs the cell autonomous behavior and places the cells in the correct embryonic context.

scholarly journals Dynamics of thin filopodia during sea urchin gastrulation

Development ◽  
1995 ◽  
Vol 121 (8) ◽  
pp. 2501-2511 ◽  
Author(s):  
J. Miller ◽  
S.E. Fraser ◽  
D. McClay
Keyword(s):  
Sea Urchin ◽  
Positional Information ◽  
Cell Interactions ◽  
Average Growth ◽  
Sea Urchin Embryo ◽  
Ligand Interactions ◽  
Patterning Defect ◽  
Mesenchyme Cell ◽  
Mesenchyme Cells ◽  
Primary Mesenchyme Cells

At gastrulation in the sea urchin embryo, a dramatic rearrangement of cells establishes the three germ layers of the organism. Experiments have revealed a number of cell interactions at this stage that transfer patterning information from cell to cell. Of particular significance, primary mesenchyme cells, which are responsible for production of the embryonic skeleton, have been shown to obtain extensive positional information from the embryonic ectoderm. In the present study, high resolution Nomarski imaging reveals the presence of very thin filopodia (02-0.4 micron in diameter) extending from primary mesenchyme cells as well as from ectodermal and secondary mesenchyme cells. These thin filopodia sometimes extend to more than 80 microns in length and show average growth and retraction rates of nearly 10 microns/minute. The filopodia are highly dynamic, rapidly changing from extension to resorption; frequently, the resorption changes to resumption of assembly. The behavior, location and timing of active thin filopodial movements does not correlate with cell locomotion; instead, there is a strong correlation suggesting their involvement in cell-cell interactions associated with signaling and patterning at gastrulation. Nickel-treatment, which is known to create a patterning defect in skeletogenesis due to alterations in the ectoderm, alters the normal position-dependent differences in the thin filopodia. The effect is present in recombinant embryos in which the ectoderm alone was treated with nickel, and is absent in recombinant embryos in which only the primary mesenchyme cells were treated, suggesting that the filopodial length is substratum dependent rather than being primary mesenchyme cell autonomous. The thin filopodia provide a means by which cells can contact others several cell diameters away, suggesting that some of the signaling previously thought to be mediated by diffusible signals may instead by the result of direct receptor-ligand interactions between cell membranes.

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