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R Kolberg

Publications and source records attributed to R Kolberg.

5 recordsLinked to original sources

Redistribution of contractile and cytoskeletal components induced by cytochalasin. I. In Hmf cells, a nontransformed fibroblastoid line.

Hmf cells are normal rat fibroblastoid cells of large size having an extensive stress fiber (cable) system. On exposure to cytochalasin D (CD), shortening and segmentation of the actin-based cables and diffusion of the normal periodic distribution of tropomyosin and myosin occur, concomitant with generalized cell retraction. During retraction, areas of extended cytoplasm may be pulled apart and torn. The actin, tropomyosin, and myosin of the stress fibers become localized in dispersed masses represented in the electron microscope as compact filamentous felt-like networks. Many of these are derived from shortening of stress fibers at their insertions into the persisting attachment plaques. In a few cells, rod-like elements of variable length remain; these are CD-resistant segments of uncontracted stress fibers. Inhibitors of energy metabolism prevent these changes. Microtubules remain unaltered but are passively displaced in the CD-deformed cells. Bundles of 10 nm filaments maintain close relations with the actomyosin masses resulting from CD-treatment. Evidence is considered for the hypothesis that cellular retraction, the apparent disorganization of stress fibers, and the redistribution of contractile proteins result from unremittent energy-dependent contraction induced by CD, and that the compact forms may be analogous to rigor complexes. A mechanism for these actions of cytochalasin is proposed.

Animals

Redistribution of contractile and cytoskeletal components induced by cytochalasin. II. In HeLa and HEp2 cells.

In HeLa and HEp2, cell lines derived from human carcinoma, application of cytochalasin D (CD) is followed in minutes by generalized cell contraction and zeiosis. Simultaneously, actin, myosin and tropomyosin, mostly from cables, become relocated in condensed masses. Most of these occupy the bases of the zeiotic knobs protruding at the cell surface. In contrast to most nontransformed cell types, in these cells both the protrusions and the contractile proteins are concomitantly translocated centripetally to the cell apex to form an aggregate of zeiotic knobs and a subjacent, membrane-associated, actin-based microfilamentous cap containing tropomyosin and myosin. The redistribution of these contractile proteins is antagonized by pretreatment with inhibitors of energy metabolism, or with cyclic adenine nucleotide. The centripetal movement appears to be guided by microtubules, which tend a radiate toward apical aggregates. Under the influence of CD 10 nm filaments associate in bundles. These processes are rapidly reversed after withdrawal of CD. The changes in distribution of actin, myosin and tropomyosin in relation to cell surface structures are considered in terms of the hypothesis that CD induces contraction of the microfilament apparatus of the cortex which, at least in part, remains tethered to plasma membrane.

Carcinoma, Squamous Cell