Intracellular signals and the regulation of cell divisio

Intracellular signals are important in the regulation of cell division. These signals appear to include rises in cytosolic calcium activity and protein phosphorylation, mediated perhaps through activation of the polyphosphoinositide (polyPI) cycle. The polyPI cycle coordinates other signals by producing two elicitors, inositol-1,4,5-trisphosphate (Insl,4,5P$sb3$) and 1,2-diacylglycerol (1,2-DAG). Insl,4,5P$sb3$, through the mobilization of calcium, and 1,2-DAG, through the activation of protein kinase C, trigger many physiological responses. In this research, the role of regulatory signals in cell division is studied through the pharmacological perturbation of their normal operation. Tradescantia stamen hair cells are used because their predictable rate of mitotic progression provides a straight-forward bioassay.;The inhibition of a rise in the cytosolic calcium level arrests stamen hair cells in metaphase and the addition of calcium reverses arrest, a result suggesting the necessity of a calcium rise during metaphase. I hypothesized that an artificial increase in cytosolic calcium before the normal rise should induce anaphase precociously. I found that treatment of stamen hair cells with ruthenium red or Bay K 8644 significantly shortens the NEBD/AO interval. Ruthenium red is a calcium translocation inhibitor and Bay K-8644 is a calcium-channel agonist. Their mechanisms of action appear to be due to disruption of cytosolic calcium homeostasis. These results further support the necessity of calcium for anaphase onset.;Neomycin, an inhibitor of the polyPI cycle, arrests cells in metaphase, and 1,2-diacylglycerol reverses the arrest. Calcium is only partially sufficient to reverse the arrest. The results suggest that protein phosphorylation by protein kinase C may participate in the metaphase/anaphase transition, and while a rise in cytosolic calcium is necessary for anaphase, it may not be sufficient for this process.;Cell plate formation in Tradescantia is disrupted by 10 mM lithium. Following lithium treatment, the cell plate disperses after normal aggregation of cell plate vesicles and the resultant cell is binucleate. Myo-inositol and calcium prevent the dispersion if added at the initial phase of cell plate formation. Thus, lithium appears to affect the coalescence of cell plate vesicles. The reversal by myo-inositol and calcium suggest that polyPI cycling regulates cell plate formation.