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  • 1
    Electronic Resource
    Electronic Resource
    Intercellular communication and tissue growth (1971)
    Springer
    The journal of membrane biology 6 (1971), S. 368-385 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary A method is described for testing communication between a normal and a cancerous cell in culture without inserting microprobes into either cell; microprobes are put into other normal cells coupled to the normal cell in question. It is shown with this method that a cell strain (class-A), of epithelial morphology, isolated from Morris' liver tumor (H-5123) fails to make communicative junctions with several types of normal cells; small inorganic ions and fluorescein do not pass from the normal cells to the class-A cells (they do pass from the normal cells to normal cells, even between normal cells of different type). The class-A cells also appear incapable of junctional communication among themselves. The cells of class-A are cancerous: they are not ‘contact inhibited’ by each other or by the normal cells and they form malignant tumors when injected into test animals. Another cell strain (class-B), of fibroblastic morphology, derived from the same liver tumor as class-A makes communicative junctions readily. This strain is ‘contact inhibited’ and does not produce tumors when injected into the animals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02116580
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  • 2
    Electronic Resource
    Electronic Resource
    Intercellular communication and tissue growth: VII. A cancer cell strain with retarded formation of permeable membrane junction and reduced exchange of a 330-dalton molecule (1976)
    Springer
    The journal of membrane biology 30 (1976), S. 175-186 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary A cancer (hepatoma) cell strain is described in which the formation of junctional membrane channels is abnormally slow. The development of electrical junctional coupling following the establishment of contact between these (reaggregated) cells is at least 15 times slower than that between their normal counterparts; and junctional transfer of fluorescein eventually develops, but only in about 5% of the contacts (as against 100% normally). This deviant membrane behavior is interpreted as a retardation in the process of accretion of junctional membrane channels. Its possible etiological role in defective growth regulation is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869666
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  • 3
    Electronic Resource
    Electronic Resource
    Experimental depression of junctional membrane permeability in mammalian cell culture. A study with tracer molecules in the 300 to 800 dalton range (1979)
    Springer
    The journal of membrane biology 50 (1979), S. 65-100 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Cell-to-cell junctional permeability in mammalian cell cultures was probed with a series of fluorescent tracers ranging 300 to 800 in molecular weight, during treatment with metabolic inhibitors, Ca-transporting ionophore, and carbon dioxide. Treatment with the combination of cyanide and iodoacetic acid (1–2mm each), but not with either one alone, caused reversible junctional blockade to all tracer molecular species, large and small. (Electrical coupling, however, persisted in a proportion of the junctions tested.) Treatment with the ionophore A23187 (2–10 μm) or with CO2 (an atmosphere of 100% CO2 equilibrated with the medium) produced selective junctional blockade: transmission of a 688 and an 817-dalton tracer was generally blocked, while that of a 376-dalton tracer and, in certain conditions, that of a 559-dalton one, persisted. The junctional effect of the ionophore required the presence of Ca in the external medium; and effective junctional blockade by CO2 required pretreatment in medium with high Ca concentration or, interchangeably, pretreatment in medium with high CO2 concentration. In one cell type, prolonged exposure to medium with high Ca concentration alone sufficed to block transmission of the 688-dalton tracer. These effects are discussed in terms of the Ca hypothesis of junctional permeability regulation. In comparison with mammalian (or other vertebrate and invertebrate) organized tissues or with insect cell cultures, the mammalian cell cultures are more resistant to junctional blockade. This difference in transmission stability is discussed in terms of intracellular Ca-buffering capacities of the junctional locales; in particular, in terms of the electron-microscopic finding in the mammalian cultures of fine, bilateral cell processes connected by gap junctions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01868788
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  • 4
    Electronic Resource
    Electronic Resource
    Intercellular communication and the control of growth: X. Alteration of junctional permeability by thesrc gene. A study with temperature-sensitive mutant Rous sarcoma virus (1984)
    Springer
    The journal of membrane biology 82 (1984), S. 191-205 
    Details
    ISSN: 1432-1424
    Keywords: cell junction ; cell-to-cell communication ; cell-to-cell channel ; gap junction ; Rous sarcoma virus ; transformation ; cancer ; growth control ; tyrosine phosphorylation ; src gene ; protein kinase ; pp60src
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary To study changes of junctional membrane permeability associated with transformation, the junctions and the nonjunctional membranes of quail embryo-, chick embryo- and mouse-3T3 cell cultures, infected with temperature-sensitive mutant Rous sarcoma virus, were probed with fluorescent-labelled glutamate. Junctional permeability fell in the transformed state. In the quail cells, the fall was detectable within 25 min of shifting the temperature down to the level (permissive) at which tyrosine-phosphorylation by the viralsrc gene product is expressed. This reduction of junctional permeability is one of the earliest manifestations of viral transformation. Normal permeability was restored within 30 min of raising the temperature to the nonpermissive level, a reversibility that could be displayed several times during the span of a cell generation. The reversal seems to reflect a reopening of cell-to-cell channels rather than a synthesis of new ones; it is not blocked by protein-synthesis inhibition. Treatments with cyclic AMP and phosphodiesterase inhibitor or with forskolin, which stimulate serine and threonine phosphorylation—the type of phosphorylation on which normal junctional permeability depends (Wiener & Loewenstein, 1983,Nature 305∶433)—did not abolish, in general, the junctional effect of the virus;src tyrosine-phosphorylation apparently overrides the junctional upregulation mediated by cyclic AMP. Nonjunctional membrane permeability was not sensibly affected by the virus. It was affected, however, by temperature: lowering the temperature from the nonpermissive to the permissive level caused the nonjunctional permeability to fall, andvice versa. This change was unrelated to transformation. Its secondary effect on junctional transfer is in the opposite direction to that produced by the temperature-activated viral transformation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01871629
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  • 5
    Electronic Resource
    Electronic Resource
    Studies on the formation of a permeable cell membrane junction (1974)
    Springer
    The journal of membrane biology 19 (1974), S. 339-355 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Coupling by permeable membrane junction between single pairs of newt embryo cells (macroblastomeres) was inducedin vitro. At the same time, the resistance of the developing cell-to-cell diffusion channels (junctional membrane) and that of their insulation from the exterior (junctional insulation) were determined by electrical measurement. From the moment the cell coupling was first detected electrically, the resistance of junctional membrane fell gradually to a relatively steady level during 0.5–1 hr. Meanwhile, the resistance of junctional insulation rose gradually to a peak, then declined somewhat to a relatively steady level. An upper limit for the steady-level resistivity of junctional membrane was estimated from measurements on partly separated cells coupled by 3–4 strands of 1 μ2 cross-section; this estimate is 10−2 Ω cm2, 6 orders of magnitude less than the resistivity of nonjunctional membrane. Viewed in the light of a model proposed earlier (W. R. Loewenstein, 1966), these results suggest that junctional coupling may develop by accretion of diffusion-channel units of ≦10−2 Ω cm2 resistivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869985
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  • 6
    Electronic Resource
    Electronic Resource
    Studies on the formation of a permeable cell membrane junction (1974)
    Springer
    The journal of membrane biology 19 (1974), S. 305-337 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Individual cells (macroblastomeres) of newt embryo were brought into contact, and electrical coupling was monitored during the formation of permeable membrane junction. In one set of experiments, the cells were allowed to establish contact at random membrane spots by spontaneously moving cell processes. Coupling became detectable 8–14 min after contact. In another set, contact was imposed, by micromanipulation, at membrane spots of known junctional history. The basic experiment was (i) to make a junction (conditioning junction) at randomly chosen membrane spots, (ii) to pull the cells apart interrupting their electrical coupling (uncoupling), and (iii) to make a new junction (test junction) either at the same spots that contained the conditioning junction or at different ones. The times required for coupling onset at test junctions fell into two classes, depending on whether in the uncoupling step the membrane continuity between the two cells had been broken or preserved. When all membrane continuity had been broken, coupling through the test junctions became detectable within 4–20 min after membrane contact. This was so when the spots of membrane contact contained conditioning junction as well as when they did not. When membrane continuity (but not coupling) had been preserved in the form of submicroscopic strands, coupling through the test junction set in within 1 sec of joining the cells at spots containing conditioning junction. This capacity for rapid coupling persisted for roughly 10 min following the uncoupling step; thereafter the time of coupling onset was of the class with broken membrane continuity. During development of junction, the coupling coefficients rose gradually over 10–30 min from the detectable level (0.03 or 0.05) to a plateau (0.3–0.9). The cells were capable of developing and of maintaining coupling throughout their entire 100-min division cycle. Treatments with colchicine (0.2–1.1mm) and with cytochalasin B (0.5–1 μm), blocking cytokinesis and division, did not prevent the development or maintenance of coupling. Treatment with dinitrophenol (1mm) prevented the development of coupling, but not that of cell adhesion, and (3mm) blocked reversibly the coupling in established junction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869984
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  • 7
    Electronic Resource
    Electronic Resource
    Intercellular communication and tissue growth (1969)
    Springer
    The journal of membrane biology 1 (1969), S. 274-293 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Epithelial cells of normal rat (adult) liver and hamster embryo in tissue culture communicate through membrane junctions: the membrane regions of cell contact are highly ion-permeable. Cancerous counterparts of these cells, cells from Morris' and Reuber's liver tumors and from x-ray-transformed embryo cultures, do not communicate under the same experimental conditions. These cells also fail to communicate with contiguous normal cells. Cancerous fibroblastic cells from a variety of tissues, including cells transformed by virus, x-radiation and chemicals, communicate as well as their normal counterparts; this is so for long- and short-term cell cultures. Communication in some fibroblastic cells is sensitive to components of blood serum: normal and transformed hamster embryo fibroblasts, which communicate when cultured in medium containing fetal calf serum, appear to lose communication in medium containing calf serum; the converse holds for hamster (adult) fibroblasts and 3T3 cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869786
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  • 8
    Electronic Resource
    Electronic Resource
    Permeability of a cell junction during intracellular injection of divalent cations (1976)
    Springer
    The journal of membrane biology 28 (1976), S. 71-86 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Divalent cations are microinjected intoChironomus salivary gland cells while the cell-to-cell passage of fluorescein (330 dalton) and electrical coupling are monitored. Injections of Ca and Mg that substantially depolarize the cells produce block or marked slowing fluorescein passage, accompanied by electrical uncoupling. Injections of Ca, Mg or Sr that cause little depolarization, and presumably smaller elevation of divalent cation concentration in the cytoplasm, produce block or marked slowing of fluorescein passage with little or no detectable electrical uncoupling. This partial uncoupling may reflect total closure of a fraction of the channels in junctional membrane or partial closure of all channels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01869691
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  • 9
    Electronic Resource
    Electronic Resource
    Intercellular communication and tissue growth: IX. Junctional membrane structure of hybrids between communication-competent and communication-incompetent cells (1977)
    Springer
    The journal of membrane biology 34 (1977), S. 39-54 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The structure of the membrane junctions of the hybrid cell system, examined in the companion paper in respect to competence for communication through cell-to-cell membrane channels, is here examined by freeze-fracture electron microscopy. The junctions of the channel-competent parent cell and of the channel-competent hybrid cells present aggregates of intramembranous particles typical of “gap junction”; those of the channel-incompetent parent cell and channel-incompetent segregant hybrid cells do not. Competence for junctional communication and for gap junction formation are genetically related. The junctions of the intermediate hybrid cells with incomplete channel-competence (characterized by cell-to-cell transfer of small inorganic ions but not of fluorescein), present special intramembranous fibrillar structures instead of discrete gap-junctional particles. The possibility that these structures may constitute coupling elements with subnormal permeability is discussed in terms of incomplete dominance of the genetic determinants of gap junction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870292
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  • 10
    Electronic Resource
    Electronic Resource
    Intercellular communication and tissue growth: VIII. A genetic analysis of junctional communication and cancerous growth (1977)
    Springer
    The journal of membrane biology 34 (1977), S. 1-27 
    Details
    ISSN: 1432-1424
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Normal, proliferating cells are interconnected at their junctions by membrane channels through which molecules can pass from cell to cell (Loewenstein, W.R. 1966.Ann. N.Y. Acad. Sci. 137:708). A channel-competent, normally growing cell (human fibroblast) was hybridized with a channel-incompetent cancer cell (mouse L-1d cell), and the segregant hybrid clones were analyzed in a genetic approach to the question of whether the junctional membrane channels are instrumental in transmission of growth-controlling molecular signals. The channel competence of the human parent was characterized by the ability to transfer small inorganic ions (electrical coupling) and fluorescein, and the growth patterns of this cell, by growthin vitro to low saturation densities and nontumorigenicity in immuno-suppressed hosts. The mouse parent cell had the opposite characteristics. The early hybrid generations (which still had a large part of each parent chromosome complement) were of two classes: one class resembled the human parent cell in channel competence,in vitro growth pattern, and low tumorigenicity within 26 days; the other class presented an intermediate expression of channel competence characterized by transfer of small inorganic ions but not of fluorescein. As the hybrid generations lost human chromosomes, there was segregation of several biochemical and morphological traits, but no segregation of channel competence and normal growth traits. Among the segregants were 22 clones which had reverted to the channel-incompetent trait of the mouse parent. In every case, reversion to the channel defect went hand in hand with reversion to the growth defect, just as, in the early-generation hybrids, correction of the channel defect went hand in hand with correction of the growth defect. Thus, the human genetic factor that corrects the channel defect of the mouse parent cell seems closely linked, if not identical, with that correcting the growth defect. This genetic correlation encourages us in the belief that the channel defect may be an etiological factor in this particular cancer form.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01870290
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