Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Embryonic Structures”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,513 records · Page 84Linked to original sources
PubMed2004

Mouse orthologue of ARX, a gene mutated in several X-linked forms of mental retardation and epilepsy, is a marker of adult neural stem cells and forebrain GABAergic neurons.

Mutations in the human ARX gene show unusually heterogeneous clinical presentations, including syndromic and nonsyndromic mental retardation, myoclonic epilepsy with spasticity, and lissencephaly with abnormal genitalia, that are believed to arise from an impairment of the embryonic mechanisms building the anterior central nervous system structures. Here, we show that the murine ortholog Arx has a highly dynamic expression pattern during both early shaping of the forebrain vesicle and later major events of neural migrations and cell-type specification. Early on, the Arx gene is specifically activated in anterior forebrain anlage. Afterward, Arx expression is confined to the telencephalic vesicles and is enhanced during differentiation of the subpallial structures of the ganglionic eminences, overlapping with Dlx2, Dlx5, and Gad1 transcriptional domains. Tangentially migrating neurons reaching the cortical plate are also Arx-positive at all embryonic stages analyzed. RNA-protein colabeling staining shows that Arx expression is maintained in the mature cortical interneurons, suggesting its involvement in the different functions of the gamma-aminobutyric acid (GABA)ergic neurons settled into the adult cerebral cortex. Finally, Arx expression is detected in the anterior subventricular layer of the adult brain, where neural stem cells have been shown to be located. Of interest, Arx expression is highly up-regulated during in vitro differentiation of pure neural stem cell cultures retrieved from adult brain. All together, these findings suggest Arx as a gene involved in the commitment of proliferating neuroblasts into a GABAergic neuronal fate. In conclusion, our mouse Arx expression data provide important further insights into the puzzling complexity of the human ARX mutation pleiotropy.

Animals↗
PubMed2006

Regulation of early Xenopus development by ErbB signaling.

ErbB signaling has long been implicated in cancer formation and progression and is shown to regulate cell division, migration, and death during tumorigenesis. The functions of the ErbB pathway during early vertebrate embryogenesis, however, are not well understood. Here we report characterization of ErbB activities during early frog development. Gain-of-function analyses show that EGFR, ErbB2, and ErbB4 induce ectopic tumor-like cell mass that contains increased numbers of mitotic cells. Both the muscle and the neural markers are expressed in these ectopic protrusions. ErbBs also induce mesodermal markers in ectodermal explants. Loss-of-function studies using carboxyl terminal-truncated dominant-negative ErbB receptors demonstrate that blocking ErbB signals leads to defective gastrulation movements and malformation of the embryonic axis with a reduction in the head structures in early frog embryos. These data, together with the observation that ErbBs are expressed early during frog embryogenesis, suggest that ErbBs regulate cell proliferation, movements, and embryonic patterning during early Xenopus development.

Amino Acid Sequence↗
PubMed1992

Apical secretion and association of the Drosophila yellow gene product with developing larval cuticle structures during embryogenesis.

The yellow (y) gene of Drosophila melanogaster is required for the pigmentation of larval and adult cuticle structures. The deduced y protein sequence includes two putative N-linked glycosylation sites and a putative signal peptide, suggesting that it might be a secreted molecule. Consistent with the characteristics of a secreted protein, our in vitro translation studies using RNA synthesised from the y cDNA demonstrate that the nascent y polypeptide is a preprotein that cotranslationally translocates into the endoplasmic reticulum (ER) membrane and becomes glycosylated. The N-terminal peptide is cleaved from the preprotein between the two alanine residues at positions 21 and 22, to release the final product into the lumen of the ER. Antibodies raised against the y polypeptide detect the protein starting at 13 h post-fertilization in epidermal cells and in the cuticle structures secreted by them that later become pigmented; in addition, yellow protein is detected in the cuticle structures associated with Keilin's organs. The embryonic beta-galactosidase staining pattern of a transgene, bearing a construct in which expression of the lacZ gene is driven by the y promoter, is also described and is similar to that of the y protein. Our results indicate that the y gene product is an apically secreted protein which becomes an immobilised structural component of the pigmented cuticle.

Amino Acid Sequence↗
PubMed1992

Transforming growth factor-beta induces selective increase of proteoglycan production and changes in the copolymeric structure of dermatan sulphate in human skin fibroblasts.

Human embryonic skin fibroblasts were pretreated with transforming growth factor-beta (TGF-beta) for 6 h and then labeled with [35S]sulphate and [3H]leucine for 24 h. Radiolabeled proteoglycans from the culture medium and the cell layer were isolated and separated by isopycnic density-gradient centrifugation, followed by gel, ion-exchange and hydrophobic-interaction chromatography. The major proteoglycan species were examined by polyacrylamide gel electrophoresis in sodium dodecyl sulphate before and after enzymatic degradation of the polysaccharide chains. The results showed that TGF-beta increased the production of several different 35S-labelled proteoglycans. A large chondroitin/dermatan sulphate proteoglycan (with core proteins of approximately 400-500 kDa) increased 5-7-fold and a small dermatan sulphate proteoglycan (PG-S1, also termed biglycan, with a core protein of 43 kDa) increased 3-4-fold both in the medium and in the cell layer. Only a small effect was observed on another dermatan sulphate proteoglycan, PG-S2 (also named decorin). These observations are generally in agreement with results of other studies using similar cell types. In addition, we have found that the major heparan sulphate proteoglycan of the cell layer (protein core approximately 350 kDa) was increased by TGF-beta treatment, whereas all the other smaller heparan sulphate proteoglycans with protein cores from 250 kDa to 30 kDa appeared unaffected. To investigate whether TGF-beta also influences the glycosaminoglycan (GAG) chain-synthesizing machinery, we also characterized GAGs derived from proteoglycans synthesized by TGF-beta-treated cells. There was generally no increase in the size of the GAG chains. However, the dermatan sulphate chains on biglycan and decorin from TGF-beta treated cultures contained a larger proportion of D-glucuronosyl residues than those derived from untreated cultures. No effect was noted on the 4- and 6-sulphation of the GAG chains. By the use of p-nitrophenyl beta-D-xyloside (an initiator of GAG synthesis) it could be demonstrated that chain synthesis was also enhanced in TGF-beta-treated cells (approximately twofold). Furthermore, the dermatan sulphate chains synthesized on the xyloside in TGF-beta-treated fibroblasts contained a larger proportion of D-glucuronosyl residues than those of the control. These novel findings indicate that TGF-beta affects proteoglycan synthesis both quantitatively and qualitatively and that it can also change the copolymeric structure of the GAG by affecting the GAG-synthesizing machinery. Altered proteoglycan structure and production may have profound effects on the properties of extracellular matrices, which can affect cell growth and migration as well as organisation of matrix fibres.

Cells, Cultured↗
PubMed1990

[Lysosomes in embryonic cell differentiation].

Lysosomes as a modeling factor of embryonal morphogenesis occupy an important place in the systemic structural and ultrastructural studies on prenatal development of man. Human embryos at the age of 6 to 10 weeks of embryonal development, obtained after interruption of normal pregnancy by the method vacuum excochleation according to Andreev. Lysosomes were investigated in cells of groups, chosen in advance, from organs with various origin and degree of cellular differentiation: neurones of the spinal cord and spinal ganglia, keratinocytes of the epidermis, epithelium of lentil vesicle, chondrocytes of Merkel's cartilage, epithelium of intestines and bronchi, hepatocytes, myoblasts, corticocytes, of coelomic fetal and definitive cortex of the adrenal, metanephros, coelomic epithelium of gonad, epithelium of Mueller's duct and Wolff's ducts, hemopoietic foci and capillary vasothelium. Lysosomes were divided into three groups: primary lysosomes, secondary autolysosomes and cytosomes. Lysosomes participate in the following processes during the course of embryonal organogenesis: 1. destruction of cells of transient embryonal organs; 2. destruction and demolition of whole cells during the course of normal embryonal development; covering with a membrane and lysis of inferior cellular organelles; 5. lysis with consecutive assimilation of cytoplasmic inclusion; lysis of secretory products.

Cell Differentiation↗
PubMedDate not supplied

Development of esterase activities in the chicken before and after hatching.

The embryonic chick has long been a model for developmental biology and has often been recommended as a model system in developmental toxicology. More recently, several investigators have shown that the chick embryo also provides a good model for identifying the neurotoxic effects of environmental pollutants, especially cholinesterase-inhibiting pesticides. Although numerous studies detail the structural development of chick embryos, few describe embryonic levels of enzyme synthesis and their changes during development. In this study, the development of esterase activity in chick embryos was measured from day 9 of incubation until 46 days after hatching. Brain acetylcholinesterase (AChE) activity was detected on day 9 of incubation at a concentration of 0.364 mumoles/min/g tissue. An increase between AChE activity and age of the embryos was observed. In the liver, the nonspecific cholinesterases (ChE) and carboxylesterase activities during incubation were not different from activities after the chicks had hatched. Plasma ChE and carboxylesterase activities did not change with age after hatching. Brain neuropathy target esterase (NTE) activity was not detected on day 9 of incubation and was extremely low (6.12 nmoles/15 min/mg protein) the next day, but increased rapidly with increasing age. This study demonstrates that chick embryos have developed esterase activities in the brain and liver by day 10 of incubation and again confirms that the insensitivity of chick embryos and young chicks to organophosphorus ester-induced delayed neurotoxicity is not due to absence of NTE. In addition, the results provide baseline data for evaluating the response of embryonic and immature chicks to neurotoxicants and teratogens.

Acetylcholinesterase↗
PubMed1989

The establishment of polarity by hippocampal neurons: the relationship between the stage of a cell's development in situ and its subsequent development in culture.

Neurons removed from the embryonic hippocampus and placed into culture develop structurally and functionally distinct axonal and dendritic processes. The central issue addressed in this study concerns the extent to which the sequence of events which results in the differentiation of neurites by hippocampal neurons in culture is influenced by the cell's state of development in situ. [3H]thymidine was administered to pregnant rats either on Embryonic Day 15 (E15) or on E18.5 to label hippocampal neurons at known stages of their development. All fetuses were sacrificed on E19. Some of the fetal brains were sectioned and examined by autoradiography to determine the location of labeled cells in the hippocampus. The remaining brains were used to prepare hippocampal cell cultures. Neurons labeled at E18.5 remained confined to the ventricular zone at E19. Those labeled at E15 had completed their migration to the cortical plate. Other data suggest that the former cells had not yet initiated process outgrowth, while the latter cells had begun to elaborate both axons and dendrites. When introduced into culture, both populations of cells developed axons and dendrites and both compartmentalized MAP2 to the dendritic domain. Moreover, despite marked differences in their developmental state at the time of introduction into culture, both underwent the same sequence of developmental events leading to axonal and dendritic development. In a few cases cells that incorporated [3H]thymidine in situ at E18.5 apparently underwent mitosis in culture. These neurons also developed axons and dendrites appropriately. These results indicate that hippocampal neurons become polarized in culture, even if they have never developed axons or dendrites in situ, and do so as efficiently as cells that have become polarized before being placed into culture. Moreover, they indicate that the same sequence of events leading to the establishment of polarity occurs for hippocampal neurons with different developmental histories prior to culturing.

Animals↗
PubMed1996

The impact of new technologies to diagnose and treat periodontal disease. A look to the future.

The last 25 years have brought unprecedented advances to our understanding of periodontal disease. Consider that in 1970 periodontitis was believed to effect most individuals over the age of 35 years, to progress steadily in an individual once initiated until teeth were lost, to be the primary cause of tooth loss in adults, to be caused by the bacterial mass accumulating on the tooth surface and subgingivally, and to involve the host in some fashion or another. In the 25 years since then, impressive research advances in the epidemiology of periodontal disease, the specific bacterial etiology of periodontal disease and the immunoinflammatory mediators of periodontal tissue destruction have greatly altered our view of periodontal disease. Thus, given these research advances in the understanding of periodontitis, what may the future hold for improved diagnosis and treatment of periodontal disease? Impressive research into new ways to diagnose the periodontal diseases is well underway. Investigators are seeking new ways to diagnose an individual's degree of risk for periodontal disease initiation, susceptibility to disease progression, level of disease "activity" and the likely response to treatment and recurrence of active disease. New diagnostic tests should greatly advance our ability to more accurately and specifically diagnose periodontal disease. The future also looks promising for new treatment strategies to slow or arrest periodontal disease progression. The bacterial specificity of periodontal disease etiology revealed since 1970 has logically led to the use of antibiotics in periodontitis treatment. In the late 1980s the concept of locally delivering antibiotics to the periodontal pocket was introduced, and subsequent clinical trials have indicated that it is possible to reduce pocket depth and inflammation with tetracycline locally delivered to the periodontal pocket. Likely, we have barely scratched the surface in studying the efficacy of locally delivery antimicrobial agents to alter the progression of periodontal disease. As new agents are developed and better delivery systems to the periodontal pocket are developed, the future should see a variety of antimicrobial agents available which can slow periodontal disease progression. The future also holds promise for slowing periodontal disease progression by blocking inflammatory pathways important in periodontal tissue destruction. Clinical trials of flubiprofen, naproxen and ketoprofen indicate that it is possible to slow periodontal disease progression with non-steroidal anti-inflammatory drugs which inhibit one destructive pathway. In addition, data from animal models indicate that chemically modified tetracycline as an inhibitor of collagenase can slow disease progression in animals. Again, we have likely only just begun to explore the wide range of molecular mediators of tissue destruction which may be targeted for blocking and thereby slow or arrest periodontal disease progression. Last, research into regenerating periodontal structures lost as a result of disease has had a noteworthy record of progress in the past 25 years. Techniques that utilize bone grafts, root treatments, tissue guiding membranes or polypeptide growth factors have ably indicated that it is possible to regenerate new attachment structures in humans. As investigators continue to unravel the mysteries of the embryonic development of the periodontium, the ability to predictably regenerate lost periodontal attachment structures holds great promise for the future.

Adult↗
PubMed2003

Organogenesis of heart-vascular system derived from mouse 2 cell stage embryos and from early embryonic stem cells in vitro.

Regenerative medical treatment with embryonic stem cells (an ES cell) is a goal for organ transplantation. Structures that are tubular in nature (i.e. blood capillaries) were induced from early embryonic stem (EES) cells in vitro using embryotrophic factor (ETFs). In addition, cardiac muscle cells could be identified as well. However, differentiation of EES cells into a complete cardiovascular system was difficult because 3 germ layer primordial organs are directed embryologically in various ways and it is not possible to guide only cardiovascular organs. Thus, we introduced ETFs after the formation of an embryoid body and were successful in cloning cell clusters that beat, thus deriving only cardiovascular organs. The application of this to the treatment of various cardiovascular diseases is promising.

Animals↗
PubMed1985

Characterization, expression, and evolution of the mouse embryonic zeta-globin gene.

We have determined the complete sequence of the embryonic alpha-like, zeta (zeta)-globin gene of the BALB/c mouse. The structure of this gene establishes the amino acid sequence of the mouse embryonic zeta-globin polypeptide chain and allows us to identify sequences within the gene that may be important for its expression. One of these is a 300-base segment that is tightly conserved between mice and humans and is located at the 5' end of the zeta-globin gene. By introducing the cloned gene into permanently transfected mouse erythroleukemic cell lines and comparing its transcript with that of zeta-globin mRNA derived from embryonic yolk sac erythrocytes, we are able to show that the cloned gene is transcriptionally active and that its transcript is correctly initiated and processed. Interestingly, the zeta-globin gene is also active when permanently transfected into an immunoglobulin-producing B-cell, a cell that presumably has tissue-specific requirements for gene expression. Further, a comparison of the amino acid coding sequence of the mouse zeta-globin gene to that of zeta-like globin genes of other species supports a revised evolutionary lineage in which goats and humans are closely related, whereas mice are further removed.

Amino Acid Sequence↗
PubMed1989

Expression of c-myb in embryonal carcinoma cells and embryonal stem cells.

Mouse c-myb has been implicated in the regulation of differentiation and proliferation of haematopoietic cells. Analysis of the chromatin structure of the promoter region of c-myb in embryonal carcinoma (EC) cells and embryonal stem (ES) cells reveals a DNAse I-hypersensitive site coincident with a site found in c-myb-expressing haematopoietic cells, but absent in murine fibroblasts (which do not express c-myb). EC and ES cells were found to express c-myb mRNA, albeit at a level lower than found in haematopoietic cells. Differentiation of ES cells into embryoid bodies resulted in an elevated level of c-myb expression.

Animals↗
PubMed1998

Dedifferentiated cardiomyocytes from chronic hibernating myocardium are ischemia-tolerant.

Left ventricular biopsies from 21 patients with clinically diagnosed chronic hibernating myocardium (CHM) were examined by light- and electron microscopy. A mean of 27% of cardiomyocytes were structurally altered and were characterized as hibernating, because of reduced amount of myofibrils and increased glycogen content. Electron microscopy of these cells showed reduction of T-tubules and numerous small mitochondria, but few changes associated with degeneration, acute ischemia or apoptosis. The structural changes found in CHM are reminiscent of dedifferentiation rather than degeneration. The expression patterns of some structural proteins show resemblance with those in embryonic cardiomyocytes. Histochemically, mitochondrial NADH-oxidase and proton translocating ATPase activities were absent, whereas cytochrome c activity was present. Intracellular calcium distribution indicated normally bound sarcolemmal calcium and absence of excess mitochondrial calcium accumulation. Nuclear chromatin ranged from normal to dispersed with only a few nuclei that were clumped. These results suggest that cardiomyocytes from human CHM hearts are structurally altered, but viable, and lack morphologic and cytochemical characteristics suggestive of apoptosis or acute ischemia.

Apoptosis↗
PubMed1999

The control of cell fate in the embryonic visual system by atonal, tailless and EGFR signaling.

We describe here the role of the transcription factors encoding genes tailless (tll), atonal (ato), sine oculis (so), eyeless (ey) and eyes absent (eya), and EGFR signaling in establishing the Drosophila embryonic visual system. The embryonic visual system consists of the optic lobe primordium, which, during later larval life, develops into the prominent optic lobe neuropiles, and the larval photoreceptor (Bolwig's organ). Both structures derive from a neurectodermal placode in the embryonic head. Expression of tll is normally confined to the optic lobe primordium, whereas ato appears in a subset of Bolwig's organ cells that we call Bolwig's organ founders. Phenotypic analysis, using specific markers for Bolwig's organ and the optic lobe, of tll loss- and gain-of-function mutant embryos reveals that tll functions to drive cells to optic lobe as opposed to Bolwig's organ fate. Similar experiments indicate that ato has the opposite effect, namely driving cells to a Bolwig's organ fate. Since we can show that tll and ato do not regulate each other, we propose a model wherein tll expression restricts the ability of cells to respond to signaling arising from ato-expressing Bolwig's organ pioneers. Our data further suggest that the Bolwig's organ founder cells produce Spitz (the Drosophila TGFalpha homolog) signal, which is passed to the neighboring secondary Bolwig's organ cells where it activates the EGFR signaling cascade and maintains the fate of these secondary cells. The regulators of tll expression in the embryonic visual system remain elusive, as we were unable to find evidence for regulation by the 'early eye genes' so, eya and ey, or by EGFR signaling.

Animals↗
PubMed1989

Expression and embryonic function of empty spiracles: a Drosophila homeo box gene with two patterning functions on the anterior-posterior axis of the embryo.

Using the even-skipped homeo box as a probe to identify diverged homeo box genes in the Drosophila genome, we isolated the empty spiracles (ems) gene. Structural and functional comparisons between ems and other embryonic patterning genes of Drosophila suggest that ems acts, in part, as a homeotic selector gene, specifying the identity of some of the most anterior head segments. Mutant embryos lacking ems protein have severe patterning defects in the anterior head and are missing tracheal structures, including the filzkörper, which are normally developed by the eighth abdominal segment. ems has two different spatial patterns of expression during embryogenesis. The early, head-specific pattern consists of a single anterior stripe at the syncytial and cellular blastoderm stages. The later, metameric pattern consists of bilateral patches of ems expression in neural and ectodermal cells of every head and body segment. Variations of the ems expression pattern in bicoid mutants suggests that the morphogen protein produced by bicoid has a concentration-dependent regulatory role in the establishment of head-specific ems expression. In contrast, the metameric ems pattern is initiated independently of bicoid protein, and ems becomes expressed at high levels in the primordia of the duplicated fïlzkörper that develop in the anterior half of bicoid mutant embryos.

Amino Acid Sequence↗
PubMed1993

Developmental aspects of Bufo bufo embryo glutathione transferases.

The expression of glutathione transferase isoenzymes has been studied during the development of Bufo bufo embryo. By analysing the GSH-affinity purified materials in terms of substrate specificities, SDS-PAGE pattern, HPLC elution profile, we conclude that, up to stage 22, no significant changes in the expression of glutathione transferases isoenzymes occurred during Bufo bufo embryo development. At stage 25 the distribution of glutathione transferases was found to be slightly different from those of all other foregoing stages. A marked decrease of embryonic glutathione transferases subunits with a parallel appearance of new structurally and immunologically different subunits was noted in toad liver and kidney. Toad ovary continued to express embryonic glutathione transferase subunits.

Animals↗
PubMed2006

Unusual N-glycan structures in alpha-mannosidase II/IIx double null embryos identified by a systematic glycomics approach based on two-dimensional LC mapping and matrix-dependent selective fragmentation method in MALDI-TOF/TOF mass spectrometry.

alpha-Mannosidase IIx (MX) is an enzyme closely related to alpha-mannosidase II (MII), a key enzyme in N-glycan biosynthesis that catalyzes the first step in conversion of hybrid- to complex-type N-glycans in Golgi apparatus. Recently we generated MII/MX double knock-out mice and found that double nulls completely lack the complex-type N-glycans (Akama, T. O., Nakagawa, H., Wong, N. K., Sutton-Smith, M., Dell, A., Morris, H. R., Nakayama, J., Nishimura, S.-I., Pai, A., Moremen, K. W., Marth, J. D., and Fukuda, M. N. (2006) Essential and mutually compensatory roles of alpha-mannosidase II and alpha-mannosidase IIx in N-glycan processing in vivo in mice. Proc. Natl. Acad. Sci. U. S. A. 103, 8983-8988). In the present study, we determined minor but unusual N-glycan structures found in MII/MX double knock-out mice. We identified such N-glycans by a systematic glycomics approach applying a two-dimensional LC mapping database and matrix-dependent selective fragmentation technique in MALDI-TOF/TOF MS, a highly sensitive and reliable technique that provides specific fragmentations enabling the determination of precise oligosaccharide structures including regioisomers (Kurogochi, M., and Nishimura, S.-I. (2004) Structural characterization of N-glycopeptides by matrix-dependent selective fragmentation of MALDI-TOF/TOF tandem mass spectrometry. Anal. Chem. 76, 6097-6101). Quantitative profiling of all N-glycan structures including minor components from MII/MX nulls, MII nulls, MX nulls, and wild-type mice at embryonic day 15.5 yielded a total of 37 species when structural heterogeneity was reduced by the removal of the sialic acids. Among six unusual N-glycan structures, two glycoforms were novel and were found only in MII/MX double nulls. We characterize such structure as pseudocomplex-type N-glycans. The present study demonstrated that use of the versatile matrix-dependent selective fragmentation method in MALDI-TOF/TOF MS greatly accelerates detailed structural analysis of a trace amount of N-glycans.

Animals↗
PubMed1964

THE STRUCTURE AND ORGANIZATION OF, AND THE RELATIONSHIP BETWEEN THE ORGANIC MATRIX AND THE INORGANIC CRYSTALS OF EMBRYONIC BOVINE ENAMEL.

Electron microscope and electron diffraction studies of developing embryonic bovine enamel have revealed the organization of the organic matrix and the inorganic crystals. The most recently deposited inorganic crystals located at the ameloblast-enamel junction are thin plates, approximately 1300 A long, 400 A wide, and 19 A thick. During maturation of the enamel, crystal growth occurs primarily by an increase in crystal thickness. Statistical analyses failed to show a significant change in either the width or the length of the crystals during the period of maturation studied. Even in the earliest stages of calcification, the crystals are organized within the prisms so that their long axes (c-axes) are oriented parallel to the long axes of the prisms but randomly distributed about their long axes. With maturation of the enamel, the crystals become more densely packed and more highly oriented within the prisms. The organic matrix in decalcified sections of enamel is strikingly similar in its over-all organization to that of the fully mineralized tissue. When viewed in longitudinal prism profiles, the intraprismatic organic matrix is composed of relatively thin dense lines, approximately 48 A wide, which are relatively parallel to each other and have their fiber axes parallel to the long axes of the prisms within which they are located. Many of these dense lines, which have the appearance of thin filaments, are organized into doublets, the individual 48 A wide filaments of the doublets being separated by approximately 120 A. When observed in oblique prism profiles, the intraprismatic organic matrix is likewise remarkably similar in general orientation and organization to that of the fully mineralized tissue. Moreover, the spaces between adjacent doublets or between single filaments have the appearance of compartments. These compartments, more clearly visualized in cross- or near cross-sectional prism profiles, are oval or near oval in shape. Therefore, the appearance of the intraprismatic organic matrix (in longitudinal, oblique, and cross-sectional prism profiles) indicates that it is organized into tubular sheaths which are oriented with their long axes parallel to the long axes of the prisms in which they are located, but randomly oriented about their own long axes, an orientation again remarkably "blue printing" that of the inorganic crystals. The predominant feature of the walls of the tubular sheaths, when viewed in cross- or near cross-section, is that of continuous sheets, although in many cases closely packed dot-like structures of approximately 48 A were also observed, suggesting that the wall of the sheaths consists of a series of closely packed filaments. The 48 A wide dense lines (filaments) representing the width of the sheath wall were resolved into two dense strands when viewed in longitudinal prism profiles. Each strand was 12 A wide and was separated by a less electron-dense space 17 A wide. The intraprismatic organic matrix is surrounded by a prism sheath which corresponds in mineralized sections to the electron-lucent uncalcified regions separating adjacent prisms. Structurally, the prism sheaths appear to consist of filaments arranged in basket-weave fashion.

Ameloblasts↗
PubMed1989

[Morphofunctional characteristics of the striated centrosome rootlets of cultured embryonic pig kidney cells].

The analysis of the centrosome structure in PK-cells has shown that the striated rootlets occur in 25-30% of the cells. Most frequently, the centrosome contains 1-2 rootlets, oriented either to the active or to the nonactive centriole. Occasionally, they occur in both the centrioles simultaneously. The presence of striated rootlets does not correlate with the presence of a primary cilium in the centrosome: there occur centrosomes with the primary cilium but without striated rootlets, and conversely: with striated rootlets but without the primary cilium.

Animals↗