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C A Erickson

Publications and source records attributed to C A Erickson.

At least 73 records · Page 4Linked to original sources
PubMed1986

Development of neural tube basal lamina during neurulation and neural crest cell emigration in the trunk of the mouse embryo.

In the trunk of higher vertebrates, the neural crest (NC) cells remain temporarily within the dorsal portion of the neural tube after fusion of the neural folds; shortly thereafter they emigrate, invading surrounding spaces and tissues. One of the factors postulated to be important in the initiation of migration of NC cells is the disruption of the basal lamina (BL) over the dorsal portion of the neural tube. It has been assumed by many that the BL must be discontinuous in order that the NC cells can leave the neural tube; and indeed, experiments performed in our laboratory, and by others, have shown that NC cells cannot penetrate an intact BL. Therefore, we have undertaken a systematic ultrastructural study to evaluate the condition of the BL during neural fold elevation and NC cell emigration. Our results show that: (i) BL surrounding the neural epithelium (NE) becomes progressively more extensive from neural fold to migratory stages. It first forms on the lateral portion of the neuroepithelium of the neural folds and then extends ventrally into the region adjacent to the notochord; (ii) BL becomes continuous beneath the epidermal ectoderm (EE) that overlies the NC cell region only during the terminal stages of NC cell emigration; (iii) BL does not form over the dorsal portion of the neural tube until NC emigration is terminated; and (iv) the morphology of the BL changes as development proceeds. We conclude that absence of a BL over the premigratory NC cell population in the trunk of mouse embryos is a necessary but not a sufficient condition for emigration to take place.

Animals↗
PubMed1986

The control of pigment cell pattern formation in the California newt, Taricha torosa.

Neural crest-derived pigment cells form species-specific patterns of pigmentation in amphibian embryos. We have characterized the appearance and changes in pigment cell distribution in the embryos of the California newt, Taricha torosa. Black melanophores first appear scattered over the surface of the somites intermingled with yellow xanthophores in stage 34/35 embryos. The melanophores then migrate either dorsally to form a dorsal stripe at the apex of the somites or ventrally along the intersomitic furrows to form a midbody stripe at the somite-lateral plate mesoderm border. Xanthophores remain between the two melanophore stripes and are also found in the dorsal fin and head. The formation of the dorsal stripe coincides with a change in melanophore tissue affinity from the surface of the somites to the subectodermal extracellular matrix (ECM). The latter substratum is the location of the cue used to organize the dorsal stripe. In addition, melanophores become elongate and highly arborized, which would allow them to extend to the region where the dorsal stripe forms. In contrast, xanthophores do not form long processes in vitro. This suggests that the ability of melanophores but not xanthophores to search for a cue at the apex of the somites may account in part for the segregation of these cells types. Melanophores and xanthophores are trapped to form the midbody stripe by the pronephric duct, which is located just beneath the ectoderm at the bases of the intersomitic furrows. Ablation of the duct prevents formation of the midbody stripe, although melanophores and xanthophores still fail to migrate ventrally over the lateral plate mesoderm. Melanophores grafted to the ventral midline fail to leave the confines of the donor tissue. This suggests that a factor in the lateral plate mesoderm in addition to the pronephric duct is inhibiting further ventral migration. There is no gross morphological difference in the organization of the subectodermal ECM dorsal and ventral to the pronephric duct as revealed by alcian blue, ruthenium red and staining with antibodies to fibronectin. We also conclude that the directed dispersal of the neural crest into the space between the somites and ectoderm is due to contact inhibition of cell movement, since T. torosa neural crest cells demonstrate contact inhibition in vitro and there are enough cells in the lateral migratory spaces to make contact events likely during dispersal.

Animals↗
PubMed1985

Tension in the culture dish: microfilament organization and migratory behavior of quail neural crest cells.

We have investigated one aspect of the migratory behavior of quail neural crest (NC) cells by comparing the organization of microfilament bundles and the ability to distort migratory substrata by NC, somite, and notochord cells in vitro. In contrast to the numerous cytoplasmic stress fibers in somite-derived fibroblasts and notochord cells revealed by rhodamine-phalloidin staining and thin-section electron microscopy, microfilaments in NC cells are restricted to the cell cortex. To test the relative degrees of tension generated by these cell types on the underlying substratum, cells were cultured in collagen gels and on distortable silicone rubber sheets. Explanted somites and notochords produced dramatic radial alignment of 750 micrograms/ml collagen gels, whereas neural crest cells only aligned gels of lower concentrations. Fibroblasts did not migrate individually from explanted somites and notochords into 250 micrograms/ml collagen gels as readily as into higher concentration collagen lattices. In contrast, neural crest cells migrated into matrices of low concentration as well as into higher concentration collagen gels. Neural crest cells and their pigmented derivatives did not distort silicone rubber sheets, whereas somite and notochord-derived fibroblasts wrinkle this substratum after 4 days in culture. Thus, the differences in organization of the actin cytoskeleton reflect the tractional force exerted by these cells on their substratum. We hypothesize that the migratory behavior of NC cells in vivo may be related to their ability to translocate through embryonic extracellular matrices while generating relatively weak adhesions with the substratum, whereas the stronger forces generated by other embryonic cell types upon the delicate extracellular matrix may restrict their migration and may be associated with other morphogenetic events.

Animals↗
PubMed1985

Control of neural crest cell dispersion in the trunk of the avian embryo.

Many hypotheses have been advanced to explain the orientation and directional migration of neural crest cells. These include positive and negative chemotaxis, haptotaxis, galvanotaxis, and contact inhibition. To test directly the factors that may control the directional dispersion of the neural crest, I have employed a variety of grafting techniques in living embryos. In addition, time-lapse video microscopy has been used to study neural crest cells in tissue culture. Trunk neural crest cells normally disperse from their origin at the dorsal neural tube along two extracellular pathways. One pathway extends laterally between the ectoderm and somites. When either pigmented neural crest cells or neural crest cells isolated from 24-hr cultures are grafted into the space lateral to the somites, they migrate: (1) medially toward the neural tube in the space between the ectoderm and somites and (2) ventrally along intersomitic blood vessels. Once the grafted cells contact the posterior cardinal vein and dorsal aorta they migrate along both blood vessels for several somite lengths in the anterior-posterior axis. Neural crest cells grafted lateral to the somites do not immediately move laterally into the somatic mesoderm of the body wall or the limb. Dispersion of neural crest cells into the mesoderm occurs only after blood vessels and nerves have first invaded, which the grafted cells then follow. The other neural crest pathway extends ventrally alongside the neural tube in the intersomitic space. When neural crest cells were grafted to a ventral position, between the notochord and dorsal aorta, in this intersomitic pathway at the axial level of the last somite, the grafted cells migrate rapidly within 2 hr in two directions: (1) dorsally, in the intersomitic space, until the grafted cells contact the ventrally moving stream of the host neural crest and (2) laterally, along the dorsal aorta and endoderm. All of the above experiments indicate that neither a preestablished chemotactic nor adhesive (haptotactic) gradient exists in the embryo since the grafted neural crest cells will move in the reverse direction along these pathways toward the dorsal neural tube. For the same reason, these experiments also show that dispersal of the neural crest is not directed passively by other environmental controls, since the cells can clearly move counter to their usual pathway and against such putative passive mechanisms.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

The retention and ultrastructural appearances of various extracellular matrix molecules incorporated into three-dimensional hydrated collagen lattices.

Artificial extracellular matrices composed of collagen, glycosaminoglycans (GAG), proteoglycans (PG), plasma fibronectin (FN), and a hyaluronate-binding protein (HABP) have been prepared that morphologically resemble embryonic extracellular matrices in vivo at the light and electron microscope level. The effect of each of the above matrix molecules on the structure and "self-assembly" of these artificial matrices was delineated. (1) Matrix components assembled in vitro morphologically resemble their counterparts in vivo, for the most part. Scanning and transmission electron microscopy indicate that under our assembly and fixation conditions, collagen forms striated fibrils that are 125 nm in diameter, FN forms 30- to 60-nm granules, chondroitin sulfate proteoglycan (CSPG) forms 27- to 37-nm granules, chondroitin sulfate (CS) assembles into 100- to 250-nm spheres, and hyaluronate (HA) appears either as granular mats when fixed with cetylpyridinium chloride (CPC) or as 1.5- to 3-nm microfibrils when preserved with ruthenium red plus tannic acid. These molecules are known to assume the same configurations in embryonic matrices when the same preservation techniques are used with the exception of FN, which generally forms fibrillar arrays. (2) Addition of various matrix molecules can radically change the appearance of the collage gels. HA greatly expands the volume of the gel and increases the space between collagen fibrils. CSPG at low concentrations (less than 1 mg/ml) and CS at high concentrations (greater than 20 mg/ml) bundle the collagen fibrils into twisted ropes. (3) A variety of assays were used to examine binding between various matrix components and retention of these components in the hydrated collagen lattices. These assays included solid-phase binding assays, negative staining of spread mixtures of matrix components, cryostat sections of unfixed mixtures of matrix components, and retention of radiolabeled matrix molecules in fixed and washed gels. A number of these binding interactions may play a role in the assembly and stabilization of the matrix. (a) HA, CSPG, and FN bind to collagen. CS appears to only weakly bind to collagen, if at all. (b) FN promotes the increased retention of HA, CSPG, and to a very small degrees, CS, in collagen gels. Conversely, the GAG increase the retention of 3H-FN in the gels. Furthermore, FN binds to HA, CS, and CSPG as demonstrated by solid surface binding assays and morphological criteria. The increased retention of GAG and CSPG by the addition of FN may be due to both stabilization of binding to the collagen and trapping of matrix complexes within the gel. (c) HA binds to both CS and CSPG.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Morphology and behavior of quail neural crest cells in artificial three-dimensional extracellular matrices.

Neural crest cells migrate extensively through a complex extracellular matrix (ECM) to sites of terminal differentiation. To determine what role the various components of the ECM may play in crest morphogenesis, quail (Coturnix coturnix japonica) neural crest cells have been cultured in three-dimensional hydrated collagen lattices containing various combinations of macromolecules known to be present in the crest migratory pathways. Neural crest cells migrate readily in native collagen gels whereas the cells are unable to use denatured collagen as a migratory substratum. The speed of movement decreases linearly as the concentration of collagen in the gel increases. Speed of movement of crest cells is stimulated in gels containing 10% fetal calf serum and chick embryo extract, 33 micrograms/ml fibronectin cell-binding fragments, 3 mg/ml chondroitin sulfate, or 3 mg/ml chondroitin sulfate proteoglycan when compared to rates of movement through collagen lattices alone. Low concentrations of hyaluronate (250-500 micrograms/ml) in a 750 micrograms/ml collagen gel do not alter rates of movement over collagen alone, but higher concentrations (4 mg/ml) greatly inhibit migration. Conversely, hyaluronate (250 micrograms/ml) significantly increases speed of movement if the crest cells are cultured in high concentration collagen gels (2.5 mg/ml), suggesting that hyaluronate is expanding spaces and consequently enhancing migration. The morphology and mode of movement of neural crest cells vary with the matrix in which they are grown and can be correlated with their speed of movement. Light and scanning electron microscopy reveal rounded, blebbing cells in matrices associated with slower translocation, whereas rounded cells with branching filopodia or lamellipodia are associated with rapid translocation. Bipolar cells with long processes are observed in cultures of rapidly moving cells that appear to be adhering strongly, as well as in cultures of cells that are stationary for long periods. These data, considered with the known distribution of macromolecules in the early embryo, suggest the following: (1) Both collagen and fibronectin can act as preferred substrata for migration. (2) Chondroitin sulfate and chondroitin sulfate proteoglycan increase speed of movement, but probably do so by decreasing adhesiveness and thereby producing more frequent detachment. In the embryo, crest cells would most likely avoid regions containing high concentrations of chondroitin sulfate. (3) Hyaluronate cannot act as a substratum for migration, but in low concentrations it can open spaces in the matrix and consequently may stimulate movement. The complex interactions of combined matr

Animals↗
PubMed1984

Embryonic fibroblast motility and orientation can be influenced by physiological electric fields.

Epithelial layers in developing embryos are known to drive ion currents through themselves that will, in turn, generate small electric fields within the embryo. We hypothesized that the movement of migratory embryonic cells might be guided by such fields, and report here that embryonic quail somite fibroblast motility can be strongly influenced by small DC electric fields. These cells responded to such fields in three ways: (a) The cells migrated towards the cathodal end of the field by extending lamellipodia in that direction. The threshold field strength for this galvanotaxis was between 1 and 10 mV/mm when the cells were cultured in plasma. (b) The cells oriented their long axes perpendicular to the field lines. The threshold field strength for this response for a 90-min interval in the field was 150 mV/mm in F12 medium and between 50 and 100 mV/mm in plasma. (c) The cells elongated under the influence of field strengths of 400 mV/mm and greater. These fibroblasts were therefore able to detect a voltage gradient at least as low as 0.2 mV across their width. Electric fields of at least 10-fold larger in magnitude than this threshold field have been detected in vivo in at least one vertebrate thus far, so we believe that these field effects encompass a physiological range.

Animals↗
PubMed1983

Negative chemotaxis does not control quail neural crest cell dispersion.

Negative chemotaxis has been proposed to direct dispersion of amphibian neural crest cells away from the neural tube (V. C. Twitty, 1949, Growth 13(Suppl. 9), 133-161). We have reexamined this hypothesis using quail neural crest and do not find evidence for it. When pigmented or freshly isolated neural crest cells are covered by glass shards to prevent diffusion of a "putative" chemotactic agent away from the cells and into the medium, we find a decrease in density of cells beneath the coverslip as did Twitty and Niu (1948, J. Exp. Zool. 108, 405-437). Unlike those investigators, however, we find the covered cells move slower than uncovered cells and that the decrease in density can be attributed to cessation of cell division and increased cell death in older cultures, rather than directed migration away from each other. In cell systems where negative chemotaxis has been demonstrated, a "no man's land" forms between two confronted explants (Oldfield, 1963, Exp. Cell Res. 30, 125-138). No such cell-free space forms between confronted neural crest explants, even if the explants are closely covered to prevent diffusion of the negative chemotactic material. If crest cell aggregates are drawn into capillary tubes to allow accumulation of the putative material, the cells disperse farther, the wider the capillary tube bore. This is contrary to what would be expected if dispersion depended on accumulation of this material. Also, no difference in dispersion is noted between cells in the center of the tubes versus cells near the mouth of the tubes where the tube medium is freely exchanging with external fresh medium. Alternative hypotheses for directionality of crest migration in vivo are discussed.

Animals↗
PubMed1983

Embryonic cell motility can be guided by physiological electric fields.

Migratory embryonic quail somitic fibroblasts display a striking sensitivity to small, steady electric fields. There are three components to their response. They begin to orient their long axes perpendicular to the field lines within 5 min of current application at the optimal field strength of 600 mV/mm. The threshold field for significant orientation in 90 min is 150 mV/mm (only 3 mV/cell width). The cells migrate toward the cathode with a similar low threshold. At field strengths greater than 400 mV/mm, the cells also elongate beginning about 1 h after field application. The importance of this embryonic cell galvanotaxis and orientation by electric fields lies in the possible utilization of this behavior both by the embryo in the guidance of embryonic cell migration in vivo and by the investigator to control cell morphology and directionality of movement in vitro in order to study mechanisms of motility.

Animals↗
PubMed1983

Substrata formed by combinations of extracellular matrix components alter neural crest cell motility in vitro.

Extracellular matrix components such as collagen, fibronectin and sulphated glycosaminoglycans can act as substrata that promote neural crest motility in vitro, in the absence of serum. The cells appear to be less adhesive and move more randomly on collagen or chondroitin sulphate substrata than on fibronectin substrata. Cells do not spread or become motile on plastic dishes to which hyaluronate has been bound, presumably owing to weak adhesion to this surface. Hyaluronate added to the medium alone has little effect on cell motility. When combinations of matrix molecules are used as substrata, however, the presence of fibronectin increases spreading, directional persistence of cell motility and speed of movement above that observed on collagen alone. When added to fibronectin, chondroitin sulphate appears to reduce adhesions slightly, since the cells are more rounded. Hyaluronate added in the medium significantly reduces the extent, speed and directionality of movement on fibronectin substrata. The presence of collagen in combination with fibronectin plus glycosaminoglycans does not have a noticeable effect on cell motile behaviour, beyond that observed with fibronectin alone. The effects of combinations of matrix compounds on neural crest cell motility are thus predictable, and can be explained in terms of the known adhesive properties and reported binding interactions of these molecules. These studies in vitro are compared with neural crest cell motility in vivo.

Animals↗
PubMed1983

An SEM analysis of neural crest migration in the mouse.

The cellular morphology and migratory pathways of the trunk neural crest are described in normal mouse embryos, and in embryos homozygous for Patch in which neural crest derivatives develop abnormally. Trunk neural crest cells initially appear in 8 1/2-day embryos as a unique cell population on the dorsal neural tube surface and are relatively rounded. Once they begin to migrate the cells flatten and orient somewhat tangentially to the neural tube, and advance ventrad between the somites and neural tube. At the onset of migration neural crest cells extend lamellipodia onto the surface of the tube while detaching their trailing processes from the lumenal surface. The basal lamina on the dorsal neural tube is discontinuous when cell migration begins in this region. As development proceeds, the basal lamina gradually becomes continuous from a lateral to dorsal direction and neural crest emigration is progressively confined to the narrowing region of discontinuous basal lamina. Cell separation from the neural tube ceases concomitant with completion of a continuous basement membrane. Preliminary observations of the mutant embryos reveal that abnormal extracellular spaces appear and patterns of crest migration are subsequently altered. We conclude that the extracellular matrix, extracellular spaces and basement membranes may delimit crest migration in the mouse.

Animals↗
PubMed1980

The deformability of BHK cells and polyoma virus-transformed BHK cells in relation to locomotory behaviour.

Several aspects of the behaviour of polyoma virus-transformed BHK cells in culture have suggested that they are more deformable than BHK cells. This possibility was tested by applying negative pressure at the cell surface by means of a micropipette. It was found that PyBHK cells in early mitosis are twice as deformable as BHK cells in the same stage. In addition, the taut, non-ruffling margins of both cell types when fully spread are much less deformable than the extending, ruffling leading lamella. The degree of deformability of these cells is correlated with the distribution and organization of microfilaments and consistent with this, deformability increases greatly in the presence of cytochalasin B. The significance of deformability studies such as these is discussed.

Animals↗
PubMed1978

Contact behaviour and pattern formation of BHK and polyoma virus-transformed BHK fibroblasts in culture.

Certain behavioural and morphological aspects of cellular transformation have been studied, using baby hamster kidney cells (BHK21/13) and polyoma virus-transformed BHK cells. BHK cellsgrow to monolayer arranged in parallel arrays, whereas the transformed cells show a much greater incidence of crisscrossing and multilayering. Time-lapse cinemicrography and scanning electron microscopy were used to examine the behaviour producing these striking differences in cellular pattern. It was found, contrary to previous thought, that in both cell lines, when contact is made ruffle to ruffle, ruffling is inhibited. When BHK cell contact each other ruffle to side, strong adhesions always occur, as evidence by a large deformation of the contacted cell margin, with accompanying paralysis of ruffling. Then, the contacting cell either changes direction, usually spreading along the side of the contacted cell, or occasionally continues to protrude and underlap the other cell, although the original adhesions are seen to remain. Transformed cells never form strong ruffle-to-side adhesions, and usually underlap each other totally. When the cells were filmed, fixed and the same cells relocated in the scanning electron microscope, neither cell type was seen to move over the surface of another (overlap). Rather, all cells crisscross by underlapping (moving under the other cell). SEM also reveals PyBHK cells to have many fewer side-to-substratum adhesions than BHK cells. The smaller number of these attachments could explain the ease with which PyBHK cells underlap.

Cell Adhesion↗
PubMed1975

Treatment of irradiation injury to the ureter by ileal substitution.

Ureteral obstruction following radiotherapy for cervical cancer is most often due to recurrent tumor. However, in a few patients ureteral stricture is secondary to radiation damage. Surgical treatment of this obstruction requires special consideration since many procedures for urinary diversion may be contraindicated in an irradiated pelvis. Ileal substitution (uretero-ileoneocystostomy) preserves renal function without resorting to external diversion of urine. A discussion of the method together with a report of 6 patients treated in this manner is presented. Results were excellent, with followup ranging from 11/2 to 4 years. A brief history of irradiation damage to the ureter and the use of small bowel as substitute ureter is discussed. Patient acceptance of this surgical approach was gratifying.

Adult↗