Fig. 7. Schematic view of steps in calmodulin redistribution under microtubule disrupting treatments. In control metaphase cells and in the stages I/II of microtubule spindle impairment, CaM preserves a ring-like structure at the spindle pole and the intensity distribution along microtubules decreases from poles to kinetochores. Stage III shows that the chromosomal matrix has divided, the kinetochores lose the metaphase alignment, tending to group around the CaM-containing cores and there is a punctate distribution of CaM, in multiple small star-like structures, associated via short residual microtubules to kinetochores/chromosomes together with the remnants of the calmodulin-microtubule polar structure. In stage IV, CaM-EGFP is close to kinetochores that are attached to the chromosome mass and tubulin is punctate. In stages V and VI (vinblastine only) there is a striking dispersion of the CaM from its accumulation sites in the cytosol and tubulin paracrystals are formed. Immunofluorescence and live cell monitoring suggest that the main mechanism of the CaM-EGFP redistribution throughout these stages is by the splitting of the pericentriolar material that contains the targets for calmodulin by shortening of the spindle microtubules until they are progressively removed.