Mitosis synchronous cell division

Synchronized cultures of Chlorella ellipsoidea were used as a model system to identify biochemical modes of action of two herbicides/ butamiphos (0-ethyl--0-(3-methyl-6-nitropheny1)-N-sec-buty1-phosphorothioamidate, formerly coded S-2846), and chlorpropham (isopropyl inch lorocarban il ate). Cell cycle studies showed that butamiphos inhibited cell division, whereas its effects on respiration and general biosynthesis were slight. Confirmatory experiments with onion root apices showed that mitosis was blocked at the metaphase and that the spindle apparatus was disrupted. 

Butamiphos seems to be a highly specific inhibitor of mitosis like colchicine. Chlorpropham inhibited cell division of a synchronized Chlorella culture. Respiration was not significantly affected. 

In some cases, changes in auxin levels show a positive correlation with changes in mitotic activity. Nishinari and Yamaki (1976) noted that, in synchronized tobacco cell cultures, there is an increase in the activity of lAA-synthesiz-ing enzymes preceding an increase in the level of auxin, and that these events occur just prior to the increase in the number of dividing cells. The authors concluded that synthesis of free lAA may initiate mitosis. A dependence of cell division on internal auxin concentration in Acer pseudoplatanus was also shown by Lequay and Guern (1977). 

A rapid interference with cellular growth processes was evident when it was shown that herpes simplex virus (HSV ) prevented cell division in synchronized HeLa cells if they were infected as little as 1 hr before mitosis was expected to begin (Stoker and Newton, 1959). 

D) to break or circumvent the dormancy, the cells enter mitosis (Bennici et al., 1982). The first and second divisions are well synchronized (Serafini-Fracassini et al., 1980) however, with further divisions, synchrony is gradually lost (Yeoman et al., 1965). Likewise, there are marked changes in the timing of the first and second cell cycles with the progression of dormancy (Bennici et al., 1982). 

While this scheme seems to account for the transitory asynchrony of the hamster-species hybrids, its application to the particular case of the hybrids of the 3460 X 2472 series encounters serious diflBculties, as follows (a) In these hybrids the lagging chromosomes are always those of the hamster parent, (b) Fifty percent of the hybrid metaphases appear synchronous, yet clones of viable hybrids are not obtained. Therefore one must assume either that synchrony of some of the first mitoses is purely fortuitous (and due to fusion of cells in the same late phase of preparation for mitosis) and is not maintained in the succeeding divisions or that the inviability of these hybrids is due to causes unrelated to the observed mitotic asynchrony. The possible nature of these causes will be discussed below. Before we do so, we would like to point out that the application of the above hypothesis to the human X mouse hybrids encounters similar difiSculties. Since, on this hypothesis, a certain fraction of hybrids must result from the fusion of cells in the same phase of the life cycle, one should find a fraction of hybrids containing the full complements of mouse and human chromosomes. In fact, however, such a condition of these hybrids appears to be ephemeral. 

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