Abstract
In recent years experimental evidences (1–5) have been accumulating on the orderly organization of the chromatin-DNA within mammalian cells from the Watson-Crick double helix (secondary structure) through successive higher order DNA foldings (nucleosome and super-nucleosome) up to a quinternary level (5), being postulated as drapery-like regular packing of 300 A° “solenoid-like” or “rope-like” fibers. While uncertainty still exists on the exact three-dimensional geometry ‘in situ’ of the latter two superstructures, there is general agreement on both the tertiary structure (wrapping of DNA around octamer histones to form the nucleosome) and on the modulation of the overall chromatin structure during cell transformation and cell proliferation. Namely the native higher order structure (5, 6, 7,) has been conclusively linked to DNA replication and mitotic condensation, through abrupt structural transitions induced by enzymatic modifications of HI histones, ions and generally by the neutralization of DNA phosphate charge (as strikingly expected from polyelectrolyte theory (8)). An increase of chromatin condensation has been also consistently associated with cell transformation (either induced by virus, chemical or spontaneously), suggesting that an higher order chromatin superpacking and a reduced chromatin template (9, 4) are a prerequisite for the expression of the transformed phenotype. This apparent paradox is however complicated by the significant chromatin modulation occuring during cell cycle progression of both normal and transformed cells, which obscure the increased condensation. It would seem indeed that only the degree of coupling between changes in nuclear morphometry (chromatin higher order structure) and changes in cell morphometry is uniquely low for individual transformed cell, being quite high for every fibroblast or normal cell (5, 10). In transformed cell, the absence of any coupling would let chromatin to progress through its cycles of condensation and decondensation regardless the shape assumed by the intact cell, including a round one as in suspension or as induced by cell-cell interaction, nutritional deprivation or cell-substrate interaction. The mechanism by which cell geometry and cell growth are respectively coupled in normal and uncoupled in transformed cells (10) was indeed suggested to be the physically (microtubules-microfilaments) or chemically induced coupling and uncoupling between nuclear morphometry and cell geometry, with the higher degree of fiber superpacking being also related to the expressions of transformed phenotypes. It would be then interesting to verify if these findings can be generalized to cell transformation induced by chemical carcinogens in VIVO, but prior to characterize its significance and specific structural-functional modification induced by chemical carcinogens (as originally reported time ago (11)), it is mandatory to know more about chromatin itself. Unperturbed rat liver cells and rat liver chromatin were mainly used as experimental models; for the purpose of comparison complementary measurements on calf thymus chromatin have been carried out.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Felsenfeld, G., 1978. Nature, 271, 115–121.
Finch, J., and Klug, A., 1976. Proc. Nat. Acad. Sci. U.S.A.? 73, 1897–1901.
Nicolini, C., and Kendall, F., 1977. Physiol. Chem. Phys. 9, 265–283.
Nicolini C., 1979. In: ‘Chromatin structure and function’. C. Nicolini ed., Plenum Publishing Co., NATO-ASI Series, pp. 613–666
Nicolini, C., 1980. Journal of Submicroscopic Cytology 12 475–505.
Ruttle, H., Baldwin, J., Mathews, A., Carpenter B., Suau, P., and Bradbury, E., 1979. In: “Chromatin structure and function’. C. Nicolini ed., Plenum Publishing Co.
Dolby, T., Belmont, A., Borun, T., and Nicolini, C., 1981. J. Cell Biolgoy 89, 78–85.
Belmont, A., and Nicolini, C., 1981. J. Theoretical Biology 90, 169–179.
Kendall, F., Beltrame, and Nicolini, C., 1979. IEEE Transactions Biomed. Eng. 26, 173–175
Nicolini, C., and Beltrame, F., 1980. Cell Biology. Intl. Reports (1982) January.
Nicolini,., Ramanhatthan, R., Kendall, F., Murphy, J., Parodi, S., and Sarma, D., 1976, Cancer Research, 36, 1725–1730.
Nicolini, C., Grattarola, M., Viviani, R, Martelli, A., Basic and Allied Histoch (1982).
Sun, T., Nishio, I., and Tanaka, T., J. Chem. Phys., 1980, 73, 5971–5.
Cavazza, B., Conio, G., Patrone, E., Pioli, F., and Trefiletti, V. 1979. Makaromol. Chem., 180, 1607–1609
Parodi, S., Carlo, P. Martelli, A., Taningher, M., Finollo, R., Giaretti, 1981 J. Mol. Biol. 147, 501–521
Gallina, V., Malvano, R., and Omini, M., 1971, Review Sci. Instrum. 42, 1607–1613.
Nicolini, C., Carlo, P., Martelli, A., Finollo, R., Bignone, F., and Brambilla, G., Journal Molecular Biology in Press.
Trefiletti, V., Martelli, A., Cavazza, B., Cuniberiti, C., Nicolini, C., and Patrone, E., Internal Report Group Biostructure, 9/81 University of Genova (1981).
Nicolini, C., Belmont, A., Parodi, A., Abraham, S., and Lessin, S., 1979. J. Histochem. Cytochem., 21, 102–113.
Nicolini, C., 1980.In: ‘Advances in neuroblastoma research’. A. Evans ed., Raven Press, New York, pp. 271–285.
Nicolini, C., Kendall, F., and Giaretti, W., 1977a. Biophys. J. 19., 163–176.
Nicolini, C., Linden, W., Zietz, S., and Wu, S., 1977. Nature 270, 607–609.
Kendall, F., Beltrame, F., and Nicolini, C., 1979. In: ‘Chromatin structure and function’. Part A., C. Nicolini ed., Plenum Publishing Co., New York-London, pp. 265–292.
Beltrame, F., Chiabrera, A., Grattarola, M., Guerrim, P., Parodi, G., Ponta, D., Vernazza, G. and Viviani, R. 2nd Annual Conference of the IEEE Engineering in Medicine and Biology Society, 1980, Washington, D.C.
Bianco, B., Drago, G., Marchesi, M., Martini, C., Mela, G., and Ridella, S. 1979. IEEE Transactions Instr. & Measur., 28, 290–294
Ridella, S., Intra, E., Mela, G., and Spiga, VI Int. Conference on Electrical Bio-impedence, 1981, Tokyo.
Nicolini, C., Carlo, P. and Ridella, S., IEEE Transactions on Biomedical Engineering, 1982, submitted.
Widnell, C., and Tata, J., Biochem. J., 1964, 92, 313, 317.
Nicolini, C., Patrone, E., Cavazza, B., Trefiletti, V., Parodi, G., and Beltrame, F., Internal Report 8/81 Group of Biostructure, University of GenovA (1981) and submitted to P.N.A.S.-U.S.A.
Miller, P. Linden, W., and Nicolini, C., Z., 1979. Naturforsch. 34, 442–448.
Dolby, T., Borun, T., Gilmour, S., Cohen, A., Zweidler, A., Miller, P., and Nicolini, C., 1979. Biochemistry. 18, 1333–1345.
Kendall, F., Beltrame, F., Belmont, A., Zietz, S., Nicolini, C., 1980. Cell Biophysics 2, 373–404.
Nicolini, C., Kendall, F., Desaive, C., and Giarretti, W., 1977c. Exp, Cell Res., 106, 199–127.
Nicolini, C., 1980. Cell Biophysics, 2, 271–290
Beal, P., Hazlewood, P., and Rao, P., Science, 1976. 192, 904–906.
Nicolini, C., Kozu, A., Borun, T., and Baserga, R., 1975. J. Biol Chem. 250, 3381–3385.
Nicolini, C., Parodi, S., Beltrame, F., and Lessin, S., In Short term Tests for Chemical Carcinogenesis, eds. S. Parodi and Santi, L., Istituto Tumori, Genova (1979)
E. Farber, in this volume.
Columbano, A., Ledda, G., Rao, P., Rajalashmi, S., and Sarma, D., in this volume.
Solt, D., and Farber, E., 1976. Nature 263, 1506–1507.
Rao, P., Hazlewood, C., and Beall, P., In Cell Growth, ed., C. Nicolini, Plenum Publishing Co. 1982. New York-London, 535–548.
Mellors, R., Kupfer, A., and Hollender, A., 1953. Cancer, 6, 376–384.
Nicolini, C., Beltrame, F., and Grattarola, H., In Cell Growth, ed. C. Nicolini, Plenum Publishing Co. New York-London (1982) 587–608.
Nicolini, C., Finollo, R., and Carlo, P., submitted to Science.
Folkman, J. and Moscona, A., 1978. Nature, 273, 345–348.
Pardell, D., Vogelstein, B., and Coffey, D., 1980. Cell, 19, 527–536.
Dulbecco, R., and Elkington, J. (1975) P.N.A.S.-USA, 72, 1584–88.
Belmont, A., Kendall, F., and Nicolini, C., 1980. Cell Biophys. (1980) 2, 165–175.
Puck, T., Waldren, C., Hsie, A., 1972. Proc. Nat. Acad. Sci. U.S.A., 68, 358.
Tanaka, T., Scientific American (1980).
Bradbury, E., and Matthews, H., in Cell Growth, ed. C. Nicolini, Plenum Publishing Co. NATO-Life Science Series (1982) 411–454.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1982 Plenum Press, New York
About this chapter
Cite this chapter
Nicolini, C. et al. (1982). Chromatin, Nuclei and Water: Alterations and Mechanisms for Chemically- Induced Carcinogenesis. In: Nicolini, C. (eds) Chemical Carcinogenesis. NATO Advanced Study Institutes Series, vol 52. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4334-9_19
Download citation
DOI: https://doi.org/10.1007/978-1-4684-4334-9_19
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4684-4336-3
Online ISBN: 978-1-4684-4334-9
eBook Packages: Springer Book Archive