Development In Normal Embryos Research Articles

The coincident time-space patterns of septate junction development in normal and exogastrulated sea urchin embryos

Earlier studies have shown that two types of septate junction are formed during early sea urchin morphogenesis. One type is the straight, unbranched, double septum septate (SUDS) which is found in the ectodermal layer throughout early development. The second type is formed only in cells which invaginate to become endoderm and to form the digestive tract. This junction is characterized by pleated, anastomosing, single septum septates (PASS). In order to ascertain in which parts of the digestive tract these junctions are formed, we studied exogastrulae because the endoderm is everted and forms constricted areas of the gut which are easily recognizable. Our results show that, in control embryos, SUDS septates are found in the mouth, esophagus and coelom and that PASS septates are found in the stomach, intestine and anus. These junctional types are also found in the same areas in exogastrulae; SUDS septates are found in the stomadeum, esophagus and coelom, and PASS septates are found in the stomach and intestine. The transition from SUDS to PASS junctions takes place within the same time period in exogastrulae as in normal embryos, i.e., from the time of mid-gastrulation through the pluteus stage. These results indicate that septate junction formation in the sea urchin embryo digestive tract may be genetically programmed in terms of both time and spatial location. This program is not altered either by the major dislocation of cells from their normal position within the embryo or from normal contacts with neighboring cells.

Ontogeny and localization of the crystallins during lens development in normal and Hy-1 (hyperplastic lens epithelium) chick embryos

A strain of chickens selected for high growth rate has been found to exhibit an anomalous eye lens morphology indicating a failure of the normal process of growth regulation. Hyperplasia of the lens epithelium and annular pad, often with fiber formation, has recently been described in day-old chicks of this strain, termed Hy-1 (Clayton, 1975). The earliest evidence of this condition in this study has been found in the 11-day embryonic Hy-1 lens. Before this time, no definitive lens abnormality could be detected histologically in the Hy-1 embryos. However, the indirect immunofluorescence technique had revealed early temporal and spatial differences with regard to the lens crystallins. Antibodies, specific for delta, cathodal beta, anodal beta and alpha crystallins, were applied to sections through the lens of 2 1/2-, 3-, 3 1/2, 4-, 5-, 8- and 16-day embryonic and 1-day post-hatch normal and Hy-1 chicks. delta crystallin appears precociously in the external layer, and alpha crystallin in the prospective fiber region, of the lens rudiment of Hy-1 embryos. Both anodal and cathodal beta crystallins are retarded, however, in their appearance in the external layer/epithelium of Hy-1 lenses. Localization of the crystallin classes within the lenses of the two strains continues to vary during lens differentiation until 1 day post-hatch, at which time and during late embryogenesis annular pad and epithelium abnormalities can be frequently be seen in the Hy-1 lens. This inability to control normal lens histogenesis thus manifests itself early as alterations in the appearance of an organ-specific gene product, the crystallins.

Facial development in normal and mutant chick embryos. I. Scanning electron microscopy of primary palate formation.

Early facial development in normal chick embryos was studied by scanning electron microscopy, and compared to the abnormal facial development of a mutant in which primary palate formation does not occur, thus resulting in bilateral cleft lip. In both normal and "cleft primary palate" mutant embryos, subsequent to the appearance of the nasal placodes, the surrounding tissues elevate to give rise to the presumptive facial primordia. As the facial primordia grow forward, they gradually assume the configuration of a square which is most pronounced at five days development. In normal embryos, the square configuration is then lost as the facial primordia become aligned in preparation for primary palate formation. The primary palate is formed at six days development by fusion of the "free-ended" medial nasal processes with the combined lateral nasal and maxillary processes across the nasal grooves. Just prior to fusion, long, slender filaments extend from the apposing surfaces of the facial primordia in the regions of prefusion contact. It is speculated that these "prefusion filaments" may function in alignment or adhesion of the facial primordia. In "cleft primary palate" embryos, facial morphogenesis appears to arrest at five days development, so that the square configuration persists. The medial nasal processes never contact the lateral nasal and maxillary processes, but instead remain separated from them by wide nasal grooves. Furthermore, facial primordia of mutant embryos do not exhibit the "prefusion filaments" characteristic of normal embryos.

Scanning electron microscopy of the bursa of fabricius from normal and testosterone-treated embryos

Scanning electron microscopy (SEM) has revealed the presence of projecting follicles (PF) and button-like follicles (BLF) in the bursa of Fabricius. This study was designed to examine the embryonic bursa with SEM to ascertain which type of follicle appears first and to compare the SEM of the bursa from normal embryos with those having received testosterone propionate (TP) on the 11th day of incubation. The bursa of the latter embryos exhibits an arrested lymphoid development. PF appeared in normal embryos by 16 days and were well developed by 18 days of embryonic development. Inter-follicular epithelium was apparent by 21 days of embryonic development in normal embryos. On the other hand, bursal follicles and interfollicular epithelium failed to form in TP birds. The TP-birds exhibited a characteristic pebble-like epithelium which may attest to the regressive influence of TP on bursal epithelium or to an arrested stage of epithelial development. The PF may lead to the development of BLF or the BLF may be derived independently of PF.

The emergence of inhibition in the chick embryo spinal cord

The onset of inhibitory systems in the lumbosacral spinal cord of the chick embryo were studied by observing the effect of locally applied strychinine on polyneuronal burst discharges recorded from the cord and sciatic nerve at various ages. This putative inhibitory blocker enhanced burst activity from 13 days on, while having no net effect before this time. Enhancement included an increase in frequency of burst discharges in all embryos. Qualitative changes in patterns of burst discharge also occurred after strychnine. In 13-day embryos, burst returned to cluster forms seen only in 11–12-day controls. In those older than 16 days, a progression from the normal random bursting to complex multicomponent bursts occurred which then evolved into less complex bursts having a much more constant interburst interval. This strychnine evoked periodicity resembling burst discharge patterns earlier in development in normal embryos (11–12 days), and transformation of burst forms in 13-day embryos supports the hypothesis that inhibition is modifying burst patterns after 12 days.

Morphology of developing heart in cardiac lethal mutant Mexican axolotls, Ambystoma mexicanum

In Ambystoma mexicanum, recessive mutant gene c results in an absence of embryonic heart function because of altered influences from surrounding tissues (Humphrey, 1972). The present light and electron microscope study compares heart development in normal and mutant embryos from Harrison stage 34 or 6 days (at which normal heart beat initiates) through stage 41 or 25 days (at which mutant embryos die). The hearts display increasing differences as development progresses, and by stage 41 mutant abnormalities are striking. The normal myocardium shows organized sarcomeres at stage 34 and numerous intercalated discs subsequently appear. By stage 41, the normal myocardium is composed of highly differentiated muscle cells and shows extensive trabeculation. The mutant myocardium throughout development remains only one cell layer thick with no indication of developing trabeculae. Mutant cells at stage 34 have a few 140 Å and 60 Å filaments along with what appear to be Z bodies. A partial organization of myofibrillar components is occasionally noted at stages 38–41; however, distinct sarcomeres are not apparent and intercalated discs are rarely seen. In general the mutant cells appear less differentiated than usual and in many respects are reminiscent of pre-heart-beat normal cells. Although most mutant cells show images characteristic of pathological conditions (e.g., pleomorphic mitochondria, membranous whorls, and numerous autophagic vacuoles), selective myocardial cell death, a phenomenon associated with normal trabeculation, is not evident. It is clear that gene c, in homozygous condition, results in an altered pattern of heart cell differentiation. The mutation, by way of abnormal inductive processes, appears to affect the synthesis and organization of heart contractile proteins.

The Ultrastructure of Myocardial Cells in Normal and Cardiac Lethal Mutant Mexican Axolotls, (Ambystoma Mexicanum)

A recessive mutation has been recently described in the Mexican Axolotl, Ambystoma mexicanum; in which the heart forms structurally, but does not contract (Humphrey, 1968. Anat. Rec. 160:475). In this study, the fine structure of myocardial cells from normal (+/+; +/c) and cardiac lethal mutant (c/c) embryos at Harrison's stage 40 was compared. The hearts were fixed in a 0.1 M phosphate buffered formaldehyde-glutaraldehyde-picric acid-styphnic acid mixture and were post fixed in 0.1 M s-collidine buffered 1% osmium tetroxide. A detailed study of heart development in normal and mutant embryos from stages 25-46 will be described elsewhere.

Morphogenesis of the eye lens in a mouse strain with hereditary cataracts.

AbstractMice carrying the gene “Shrivelled, ” also known as “Cataract‐Fraser” or “Cataracta hereditaria subcapsularis, ” invariably develop lens opacities which are visible when the animals open their eyes on the fourteenth postnatal day.Lens development in normal and mutant embryos is the same until day 14 of gestation. At this stage the nuclei of the lens fibers in the controls are large and vesicular with prominent nucleoli. In the mutants the centrally located nuclei are smaller and darker with indistinct nucleoli. The nuclei of normal fibers remain large and open even after birth; those in the mutants continue to undergo pyknosis after passing through the equatorial zone in the regular fashion. The nuclear degeneration is followed, with a delay of about 24–48 hours, by swelling and vacuolization of the fibers concerned. In the adult the lens core forms an amorphous eosinophilic mass or may partly be resorbed. The cortical fibers remain normal. Anterior polar cataracts develop: the epithelial cells proliferate to form multiple layers of atypical cells, surrounded by lens capsule‐like material.The fiber degeneration may be caused by precocious cessation of protein synthesis after the cell nucleus becomes defunct. The late epithelial aberrations may be secondary to the changes in the underlying fibers and are possibly related to the reactivation of cell replication in the central part of lens epithelium seen after traum.

Some aspects of the relationship of RNA metabolism to development in normal and mutant mouse embryos cultivated in vitro

Some aspects of the relationship of RNA metabolism to development in normal and mutant mouse embryos cultivated in vitro