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PubMed1993

Gap junctional intercellular communication and connexin expression in normal and SV 40-transformed human liver cells in vitro.

The gap junction intercellular communication (GJIC) capacity of two normal human liver-derived epithelial cell strains and their SV40 large T oncogene-transformed counterparts was examined. In homologous cultures the GJIC capacity of the transformed cells was considerably less than the parental cells. In heterologous cultures, transformed cells appeared to be able to form GJIC channels with normal cells. Only non-transformed cells expressed connexin (cx) 43 gene and cx 26 or cx 32 transcripts were not detectable in any cell strains tested. When GJIC was assayed in the presence of the phorbol ester tumour promoter 12-O-tetradecanoylphorbol-13- acetate (TPA), all four strains showed a marked sensitivity to TPA in inhibitory activity at 1-10 ng/ml. In contrast to a rat liver epithelial cell line, this effect of TPA did not appear to become refractory even after 24 h exposure. These studies demonstrate that GJIC of human liver cells in culture can be decreased by viral oncogene and tumour promoter action. Such disturbance may be an important component of the carcinogenic activity of these agents.

Adult↗

PubMed1997

Down-regulation of gap junctional intercellular communication between osteoblastic MC3T3-E1 cells by basic fibroblast growth factor and a phorbol ester (12-O-tetradecanoylphorbol-13-acetate).

To address the relation between osteoblast growth and cell-to-cell communication, we examined the effects of basic fibroblast growth factor (bFGF) and 12-O-tetradecanoylphorbol-13-acetate (TPA), both potent stimulators of osteoblastic proliferation, on gap junctional intercellular communication between osteoblastic MC3T3-E1 cells. The level of intercellular communication was estimated by a photobleaching method. TPA inhibited the degree of intercellular communication in two different time-dependent manners. The early (< 1 h) inhibition by TPA was consistent with an increase in the phosphorylation of connexin 43 (Cx43). The later inhibition was caused by reduction in the total amount of Cx43 on the plasma membrane, due to the decrease in the level of Cx43 transcripts. These qualitative and quantitative modulations by TPA were inhibited by a selective inhibitor of protein kinase C, GF109203X. bFGF also attenuated the gap junctional intercellular communication. However, short exposure (< 5 h) to bFGF did not affect the communication. The fact that the growth factor immediately stimulated the phosphorylation of Cx43 indicates that the phosphorylation site(s) affected by bFGF was not involved in the inhibition of communication. The decrease in the intercellular communication level was detected by the longer exposure (> 8 h) to bFGF and paralleled the decline in the Cx-mRNA level. This inhibitory effect of bFGF was abolished by the addition of a tyrosine kinase inhibitor, herbimycin A. Thus, gap junctional intercellular communication between osteoblasts was down-regulated by osteoblastic mitogens through different mechanisms of the modulation of Cx43.

3T3 Cells↗

PubMed1989

Gap-junctional intercellular communication in epidermal cell lines from selected stages of SENCAR mouse skin carcinogenesis.

Homologous and heterologous gap-junctional intercellular communication (IC) was characterized in a panel of cell lines derived from selected stages of SENCAR mouse skin carcinogenesis. This panel included a "carcinogen-altered" cell line, 3PC, obtained from Ca2+-resistant primary adult keratinocytes after exposure to dimethylbenz(a)anthracene as well as cell lines obtained from early and late-stage papillomas and a squamous cell carcinoma (CA3/7) generated during standard in vivo initiation/promotion protocols (dimethylbenz(a)anthracene/12-O-tetradecanoyl-phorbol-13-acetate). Also studied was a cell line (B66BA) obtained from a metastatic lesion following benzo(a)pyrene-induced skin tumorigenesis. Intercellular communication was measured in low-calcium (0.05 mM) medium by quantitation of cell-cell transfer of microinjected fluorescent dye Lucifer Yellow CH. Homologous IC ability diminished progressively from 68 dye-coupled cells per injection for 3PC cultures, to between 21 and 54 dye-coupled cells per injection for three papilloma-derived cell lines, to six and three dye-coupled cells per injection for CA3/7 and B66BA cells, respectively. To test communication of these cells with their normal counterparts, heterologous IC was examined in cocultures with primary adult keratinocytes. Under the conditions used, normal cells established functional communication channels with each cell line tested, showing no selectivity. These results suggest that progressive loss of homologous but not heterologous IC capacity accompanies neoplastic development in mouse skin carcinogenesis.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1983

Changes in intercellular junctions. II. Modulation in embryonic chick liver in vitro by cytosine arabinoside and dexamethasone.

We have used an in vitro model to investigate the relationship between cell proliferation, cell maturation, and intercellular junctional changes that are seen during normal liver development. Chick liver fragments of embryonic stages 21, 28, and 39 were grown in organ culture in Medium 199 with 10% bovine serum albumin for 24 hr. Concurrent cultures were treated with cytosine arabinoside (ara-c, 20 micrograms/ml) to inhibit cell proliferation or with dexamethasone (2 microns/ml) to promote cell maturation. Control and treated liver cultures were analyzed using autoradiography to determine labeling index and quantitative computer graphic analysis of freeze-fracture micrographs to evaluate junctional changes. Explants treated with ara-c had a near zero labeling index. Those from embryonic stage 21 showed a 4-fold increase in tight junctional area, while those from embryonic stage 28 showed a 2.5-fold increase in tight junctional area and a 5-fold increase in gap junctional area. In liver of embryonic stage 39, junctional area increased, and conformation of junctions took on the typical form seen in the liver of the hatched chick. Thus high mitotic activity appears to disrupt cell junctions, reducing the amount of junctions present and causing pleomorphic configurations. Junctional area could also be modified with no change in mitotic activity by treatment with dexamethasone. Stage 28 embryo livers in culture with dexamethasone showed a 4-fold increase in the amount of tight junctions with no change in the amount of gap junctions. Some major findings based on these age-dependent responses are (1) if mitosis is blocked in young embryonic stages when proliferation is high, intercellular junctions tend to increase in amount, and to be more mature in configuration; (2) if maturation is stimulated with no change in proliferation, those junctions which normally increase with differentiation will increase in amount; and (3) it is possible to produce a change in the amount of one junctional type without affecting the other. Therefore the amount of cell surface occupied by junctions at any given time seems to depend on both the pattern of synthetic activity in the cell and the degree to which cell to cell contacts are stable and undisrupted by mitotic activity.

Animals↗

PubMed2001

Role of PKC and MAP kinase in EGF- and TPA-induced connexin43 phosphorylation and inhibition of gap junction intercellular communication in rat liver epithelial cells.

Gap junction intercellular communication (GJIC) is involved in the regulation of many cellular processes. The gap junction channels are made up of connexins and the flow of polar low molecular weight molecules through these channels is inhibited by several groups of substances, such as tumour promoters and growth factors. The phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), chlordane and the growth factor epidermal growth factor (EGF) are potent inhibitors of GJIC in several cell types, including the rat liver epithelial cell line IAR6.1. The induced inhibition of communication by TPA and EGF in IAR6.1 cells is associated with hyperphosphorylation of connexin43, the connexin responsible for GJIC. Two enzyme inhibitors, PD98059, a specific inhibitor of MEK kinase, and GF109203X, a selective inhibitor of protein kinase C (PKC), were used to study the signalling pathways involved in the effect of EGF and TPA on GJIC, with the following conclusions. The inhibition of cell communication in IAR6.1 cells by EGF is likely to be mediated by direct phosphorylation of connexin43 by MAP kinase. TPA blocks GJIC mainly by the direct action of PKC, but also partly through cross-talk with the MAP kinase pathway. Connexin43 hyperphosphorylation induced by TPA is, as for EGF, mediated through MAP kinase, while PKC seems to block GJIC either through other substrates or induces a type of connexin43 phosphorylation that causes no significant electrophoresis mobility shift.

Animals↗

PubMed1982

Intercellular junctions between specialized ependymal cells in the subcommissural organ of the rat.

The permeability of intercellular junctions in specialized ependymal cells in the rat subcommissural organ (SCO) has been studied ultrastructurally by freeze-fracturing and tracer experiments with horseradish peroxidase (HRP). In addition to normal smooth membrane, areas which could be classified as a leaky tight junction are found within the ependymal junctional region. This consists of only one or two relatively continuous strands but with interruptions in the apical portion. Some strands are perpendicular to the apical membrane surface and often form hairpin-like bends in the basal portion of the junction. The junctional region also shows areas with no strands but only a rippled membrane structure which may be equivalent to very close appositions without fusion of adjacent ependymal cell membranes. The relative proportions of normal smooth membrane, strands and rippled structure in the junctional region is approximately 3:4:6 including two parts overlapping of the strands and rippled structure. Intraventricularly infused HRP passes through many junctions but is occasionally stopped, leaving unstained intercellular spaces of various lengths between membrane fusions of tight junctions. Even when it is stopped, the intercellular space below the junction is densely stained by the enzyme. Orthogonal arrays of intramembrane particles are found to be distributed on the basal and lateral cell membranes below the junctional region in the SCO ependyma.

Animals↗

PubMed1993

Electron microscopic demonstration of intercellular junctions between subendocardial smooth muscle and myocardium in the sheep heart.

The eustachian ridge of 11 sheep hearts was examined by light and electron microscopy to elucidate the morphologic relationship between cardiac smooth muscle cells and myocardial cells. Smooth muscle cells were commonly observed in the subendocardial connective tissue and they were usually arranged in strands. When mixed with myocardial cells at the margin of these strands, smooth muscle cells exhibited numerous direct connections with the myocardial cells. These intercellular junctions were composed primarily of simple appositions (undifferentiated regions), but occasional desmosomes and fasciae adherents (intermediate junctions) were seen. We found no nexus (gap junctions) at these sites. The existence of direct intercellular junctions between smooth muscle and myocardium suggests several possible electrical and mechanical interactions.

Animals↗

PubMed1982

Intercellular junctions in the hematopoietic compartments of embryonic chick bone marrow.

Avian embryonic marrow is segregated into distinct erythropoietic and granulopoietic compartments. Within each compartment presumptive stem cells and immature blood cells establish intimate contact with their respective stromal cell. In this study we have examined one aspect of potential hematopoietic cell-stromal cell interaction by looking for the presence of intercellular junctions between these two elements. In previous studies, after aldehyde fixation, junctions were not observed, but after perfusion fixation with tannic acid-glutaraldehyde, pentilaminar junctions became evident. These junctions were most characteristically located in the intravascular erythropoietic compartment, but were also found in the extravascular granulopoietic compartment. Junctions frequently joined presumptive stem cells with sinusoidal endothelial cells as well as joining immature erythroblasts with sinusoidal endothelial cells; and less frequently, junctions connected adjacent erythroid cells. However, reticulocytes and erythrocytes were never seen to have formed junctions with any other type of cell. Similar junctions within the extravascular compartment connected contiguous reticular cells and also, on occasion, reticular cells with sinusoidal endothelial cells. Hematopoietic cell-reticular cell junctions were restricted to two classes of blood cells--extravascular presumptive stem cells and mast cells. There was no evidence of junctions connecting mature or maturing granuloid cells and any other cell type. The presence of intercellular junctions between immature blood cells and their respective stromal cells suggests that such interactions might play an important role in avian hematopoiesis. However, further work will be needed to determine if these junctions are merely adherence sites or whether they represent sites of intercellular communication. In either event, these junctions appear to reflect a mechanism whereby the marrow stroma could regulate erythroid maturation.

Animals↗

PubMed1987

Intercellular junctions between fibroblasts in connective tissues of the eye of macaque monkeys. A thin section and freeze fracture analysis.

Thin-section electron microscopy and freeze fracture were used in the analysis of the intercellular junctions between fibroblasts in connective tissues of the eye of Macaca mulatta, M. fascicularis, and M. arctoides. Fibroblasts located in the subconjunctival loose connective tissue, anterior sclera, scleral spur, iris stroma, ciliary body stroma, and posterior choroid were jointed by three kinds of junctions. Gap junctions were of different sizes and frequently composed of a small number of connexons organized in polygonal aggregates or linear arrays. Tight junctions were represented by isolated strands and never composed a continuous belt around the cells. Intermediate junctions were seen in thin sections but did not have any representation in the interior of the plasma membrane. It remains to be established whether, as is the case in other tissues, pathologic conditions of the eye are accompanied by some changes in the morphology and distribution of intercellular junctions between fibroblasts.

Animals↗

PubMedDate not supplied

Role of protein kinase C in the deficient gap junctional intercellular communication of K-ras-transformed murine lung epithelial cells.

BACKGROUND: Protein kinase C (PKC) activity is increased and gap junctional intercellular communication (GJIC) is decreased frequently in Ras-transformed cells. We investigated the roles of Ras and PKC in the deficient gap junctional intercellular communication (GJIC) of K-ras-transformed E9 mouse lung carcinoma cells. METHODS: GJIC was measured by fluorescent dye microinjection. Ras activity was blocked with lovastatin or a K-ras antisense oligonucleotide. PKC activity was inhibited with GF 109203X or apigenin or was downregulated by overnight treatment with 12-O-tetradecanoylphorbol-13-acetate. The content and phosphorylation of the gap junction protein, connexin43 (Cx43), was assessed by Western blot. RESULTS: E9 cell GJIC was increased two-three fold by lovastatin, the K-ras antisense oligonucleotide, and PKC inhibition/downregulation. Cx43 content and phosphorylation were unchanged, however. CONCLUSIONS: Oncogenic Ras blocks GJIC in E9 cells through a PKC-dependent mechanism, but this does not directly involve Cx43 expression or phosphorylation.

Animals↗

PubMed1997

Changing patterns of gap junctional intercellular communication and connexin distribution in mouse epidermis and hair follicles during embryonic development.

In the mouse embryo between embryonic days 12 (E12) and 16, regular arrays of epidermal placodes on the mystacial pad develop into whisker follicles. This system was chosen for analysis of gap junctional intercellular communication during differentiation. The patterns of communication were studied by microinjection of the tracers Lucifer yellow-CH (LY-CH) and neurobiotin (NB), while immunofluorescent staining was used to study distribution of connexins 26 and 43. Extensive communication was seen between keratinocytes in developing hair pegs or, in later-stage hair follicles, in the germinative matrix. Coupling between adjacent hair pegs via interfollicular epidermis was not observed. Coupling also became restricted as follicular cells differentiated to form outer root sheath, inner root sheath, and hair shaft. Extensive gap junctional coupling is characteristic of keratinocytes that are rapidly proliferating (as in hair pegs and germinative matrix). Follicular keratinocytes commence differentiation shortly before restriction of gap junctional coupling becomes evident. Dermal mesenchymal cells undergoing different modes of differentiation also exhibit differences in gap junctional coupling, as evidenced by poor transfer of LY-CH between cells in dermal condensations of hair follicles compared with extensive transfer elsewhere in the dermis. LY-CH and NB were not transferred between epidermal or follicular epithelium and mesenchyme, arguing against a direct role for gap junctions permeable to known second messenger molecules or nucleotides in epithelial-mesenchymal interactions in this system. The distribution of connexins 26 and 43 in epidermis and hair follicles changed during differentiation but there was no correlation with changing patterns of dye transfer, indicating an unexpected degree of complexity in the relationship between gap junctional intercellular communication and connexin protein distribution during development.

Animals↗

PubMed1977

Intercellular junctions of antennal gland epithelial cells in the crayfish, Orconectes virilis. A freeze-fracture study.

Labyrinth and nephridial canal cells of the crayfish (Orconectes virilis) antennal gland possess two types of intercellular junctions revealed by freeze-fracture studies. Apical margins of the cells are connected by long septate junctions. In replicas, these junctions consist of many parallel rows of 80--140 A intramembrane particles situated on the PF membrane face (EF and PF fracture faces of Branton et al., 1975). Rows of pits are found on the EF fracture face and are deemed complementary to the rows of particles. Moreover, lateral margins of basal regions of the epithelial cells are attached by many intercellular junctions. These contacts are characterized in thin plastic sections by a narrow dense cytoplasmic plaque located subjacent to the plasma membrane at sites of adjoined cells, and 5 to 12 fine strands of dense material that extend across the intercellular gap between adjoined cells. In freeze-fracture replicas, EF intramembrane faces basal to the region of the plasma membrane containing septate junctions exhibit numerous discoid clusters of particles. The particle aggregates, assumed to represent freeze-cleave images of adhering junctions, range from 900 to 3,700 A in diameter, with individual particles about 185 A in diameter. These junctions appear to connect epithelial cell processes formed by basal infoldings of the plasmalemma, and occur between adiacent cells as well as adiacent processes of a single cell. The discrete aggregates of particles resemble replicated desmosomes (Shienvold and Kelly, 1974) and hemi-desmosomes (Shivers, 1976); therefore, they probably do not constitute a basis for electrical coupling between antennal gland epithelial cells.

Animals↗

PubMed2001

Neutrophil transmigration in inflammatory bowel disease is associated with differential expression of epithelial intercellular junction proteins.

Inflammatory bowel disease (IBD) consisting of ulcerative colitis (UC) and Crohn's (CD) typically displays a waxing and waning course punctuated by disease flares that are characterized by transepithelial migration of neutrophils (PMN) and altered barrier function. Since epithelial barrier function is primarily regulated by the apical most intercellular junction referred to as the tight junction (TJ), our aim was to examine expression of TJ and adherens junction (AJ) proteins in relation to PMN infiltration in mucosal tissue samples from patients with active IBD. Expression of epithelial intercellular TJ proteins (occludin, ZO-1, claudin-1, and JAM) and subjacent AJ (beta-catenin and E-cadherin) proteins were examined by immunoflourescence/confocal microscopy, immunohistochemistry, and Western blotting. Colonic mucosa from patients with UC revealed dramatic, global down-regulation of the key TJ transmembrane protein occludin in regions of actively transmigrating PMN and in quiescent areas in the biopsy samples. Significant decreases in occludin expression were observed at the protein and mRNA levels by Western and Northern blotting. In contrast, expression of other TJ and AJ proteins such as ZO-1, claudin-1, JAM, beta-catenin, and E-cadherin were down-regulated only in epithelial cells immediately adjacent to transmigrating PMN. Analysis of inflamed mucosa from Crohn's disease patients mirrored the results obtained with UC patients. No change in TJ and AJ protein expression was observed in colonic epithelium from patients with collagenous colitis or lymphocytic colitis that are respectively characterized by a thickened subepithelial collagen plate and increased intraepithelial lymphocytes. These results suggest that occludin expression is diminished in IBD by mechanisms distinct from those regulating expression of other intercellular junction proteins. We speculate that down-regulation of epithelial occludin may play a role in enhanced paracellular permeability and PMN transmigration that is observed in active inflammatory bowel disease.

Adherens Junctions↗

PubMed1988

Loss of intercellular junctional communication correlates with metastatic potential in mammary adenocarcinoma cells.

A series of rat 13762NF mammary adenocarcinoma cell sublines and clones of various spontaneous pulmonary metastatic potentials from the mammary fat pads of syngeneic rats were examined for their intercellular junctional communication. Using the scrape-loading dye-transfer technique to introduce Lucifer yellow (Mr 457) into cells, we measured the abilities of 13762NF cells to transfer dye to adjacent cells. There was an excellent correlation between loss of Lucifer yellow dye transfer and spontaneous metastatic potential (average total volume of lung metastases inversely correlated to % cells coupled, r = 0.93; average total number of lung metastases inversely correlated to % cells coupled, r = 0.91). The data suggest that high metastatic potentials are closely correlated with loss of intercellular junctional communication in these malignant mammary tumor cells.

Adenocarcinoma↗

PubMed1992

Inhibitory effects of endosulfan on gap junctional intercellular communication in WB-F344 rat liver cells and primary rat hepatocytes.

The chlorinated cyclodiene insecticide endosulfan is a potent inhibitor of gap junctional intercellular communication (GJIC) in vitro, a property shared by many tumour promoters and suggested to indicate an intrinsic tumour-promoting potential. However, endosulfan did not act as a tumour promoter in an altered hepatic foci assay in the rat in vivo, and ambiguous results regarding the carcinogenic potential of endosulfan have emerged from long-term studies in rodents. In the present study the GJIC-inhibitory potentials of the two isomers of endosulfan were investigated in WB-F344 rat liver epithelial cells and primary rat hepatocytes. The results show that both isomers are inhibitors of GJIC. However, beta-endosulfan (ENDO beta) is a more potent inhibitor of GJIC in primary rat hepatocytes than alpha-endosulfan (ENDO alpha), whereas the two isomers were equally potent as inhibitors of GJIC in WB-F344 rat liver cells. In primary rat hepatocytes membrane-permeant dibutyryl cyclic AMP (dB-cAMP) counteracts the inhibitory effect of ENDO beta without affecting the effect of ENDO alpha. However, in WB-F344 rat liver cells dB-cAMP failed to prevent the inhibitory effects of either ENDO alpha or ENDO beta. In addition, studies in WB-F344 rat liver cells show that ENDO alpha beta does not decrease the intracellular cAMP concentration. Thus, it is unlikely that ENDO alpha beta or its isomers and metabolites inhibit GJIC by lowering the intracellular cAMP concentration. Furthermore, comparison of the effective doses and recovery times imply that GJIC in WB-F344 rat liver cells is more sensitive to treatment by ENDO alpha beta, its isomers and metabolites than GJIC in primary rat hepatocytes. Thus, the present results demonstrate significant differences between primary rat hepatocytes and WB-F344 rat liver cells in the response of their GJIC to endosulfan.

1-Methyl-3-isobutylxanthine↗

PubMed2006

Connexin expression and gap junctional intercellular communication in human squamous cell carcinoma of the head and neck.

OBJECTIVE: Our laboratory is investigating the role that gap junction intercellular channels (composed of proteins called connexins) play in communicating apoptotic signals from therapeutically targeted squamous cell carcinoma of the head and neck (SCCHN) cells to adjacent, untreated, "bystander" cells (bystander effect). The nature of this research underscores the importance of delineating connexin expression patterns in SCCHN, and how this correlates with gap junctional intercellular communication (GJIC) and bystander effects. STUDY DESIGN: The GJIC activity of a diverse panel of SCCHN cell lines, as well as normal oral epithelial (NOE) cell controls was determined in vitro. These data were correlated with connexin expression patterns determined through connexin 43 and connexin 26 immunofluorescence. RESULTS: Cell lines with retained GJIC activity all expressed connexin 43 on the cell membrane. Cell lines that did not communicate microinjected lucifer yellow (lost GJIC activity) showed no connexin expression, either at the cell membrane or in the cytosol. Connexin 26 was not expressed in any of our SCCHN cell lines, whereas both connexin 43 and connexin 26 were expressed in the NOE cell controls. Furthermore, connexin 43 introduction into a GJIC (and connexin) deficient SCCHN cell line conferred no growth inhibitory effect. CONCLUSION: Connexin 43 expression correlates with retained GJIC in SCCHN in vitro. Connexin 26 may have a role as a tumor suppressor in SCCHN. SIGNIFICANCE: The data presented have relevance to our ongoing investigations of gap-junction mediated bystander effects in SCCHN and are being expanded to investigations on actual SCCHN tumor specimens.

Apoptosis↗

PubMed2001

[Effect of transfected Cx43 gene on the gap junction intercellular communication and the human glioma cells proliferation].

OBJECTIVE: To investigate the role of connexin 43 (Cx43) gene in the gap junction intercellular communication (GJIC) and the development of glioma so as to demonstrate the feasibility of using Cx43cDNA as the target of gene therapy for gliomas. METHODS: TJ905 human glioblastoma cell line without Cx43 gene expression was transfected with Cx43cDNA mediated by lipofectamine. Northern blot, in situ hybridization and immunocytochemistry were used for examination of Cx43mRNA and its protein examination; MTT assay and silver colloid stain were used to detect cell proliferation. TUNEL method was used to determine the cell apoptosis. Scrape loading dye transfer (SLDT) was used to monitor GJIC. RESULTS: The TJ905 transfectants resulted in dramatic upregulation of Cx43mRNA and its protein, with the GJIC of transfected glioma cells restored. Clones with high Cx43 expression also showed reduced proliferation in vitro. However, the cell apoptosis did not increase following the transfection with Cx43 gene. CONCLUSION: These results indicate that Cx gene and gap junction intercellular communication are of crucial importance in malignant glioma cell growth and development. Cx43 gene may be a target for gene therapy of gliomas.

Blotting, Northern↗

PubMed1978

Freeze-etching observation on the development of intercellular junctions of the duodenal epithelial cells in the chick embryo.

Development of intercellular junctions in duodenal epithelium in the chick embryo was studied by electron microscopy using the thin-section and freeze-fracture techniques. Incomplete tight junctions are already seen in 6 and 7 day old embryos at the apical portion of the lateral plasma membrance, and consist of 1-7 strands, their mean depth measuring 0.2 micron. This corresponds to a "very leaky type" (CLAUDE and GOODENOUGH) of tight junction. Ridges on the PF are discontinuous and rarely cross or link. The tight junctions extend basally at the place where more than three epithelial cells are in contact. On the lateral plasma membrane, particle-aggregates suggesting primitive gap junctions are already recognized. Some are dense aggregations of 3-5 membrane-particles with a halo free of the particles and others are rather loose aggregations of 5-10 particles with an indistinct halo. In 9 day old embryos, the ridges of the tight junction become more discontinuous, although the frequency of the linkage of the neighboring ridges increases. The compartments bounded by the tight junctional strands are angular. These strands become continuous and the facets surrounded by them are roundish in 12 day old embryos. The presumptive immature gap junctions show a characteristic polygonal pattern in 9 day old embryos and gradually increase in size. Mature tight junctions and typical gap junctions of 0.3-0.4 micron diameter are seen after 18 days of incubation. The strands number 6-8 and the depth of the tight junction measures about 0.4 micron in 18 day old embryos. In the chick embryo duodenal epithelium, the tight and gap junctions develop independently from each other without any direct interaction between them.

Animals↗