Most animal cells divide symmetrically: the contractile ring forms around the equator of the parent cell, producing two daughter cells of equal size and with the same components. This symmetry results from the placement of the mitotic spindle, which in most cases tends to center itself in the cytoplasm. Astral micro-tubules and motor proteins that either push or pull on these microtubules contribute to the centering process.
There are many instances in development, however, when cells divide asymmetrically to produce two cells that differ in size, in the cytoplasmic contents they inherit, or in both. Usually, the two different daughter cells are destined to develop
Figure 17–49 The special features of cytokinesis in a higher-plant cell. The division plane is established before  m phase by a band of microtubules and actin filaments (the preprophase band) at the cell cortex. at the beginning of telophase, after the chromosomes have segregated, a new cell wall starts to assemble inside the cell at the equator of the old spindle. The interpolar microtubules of the mitotic spindle remaining at telophase form the phragmoplast. The plus ends of these microtubules no longer overlap but end at the cell equator. golgi-derived vesicles, filled with cell-wall material, are transported along these microtubules and fuse to form the new cell wall, which grows outward to reach the plasma membrane and original cell wall. The plasma membrane and the membrane surrounding the new cell wall fuse, separating the two daughter cells.
along different pathways. To create daughter cells with different fates in this way, the mother cell must first segregate certain components (called cell fate determinants) to one side of the cell and then position the plane of division so that the appropriate daughter cell inherits these components (Figure 17–50). To position the plane of division asymmetrically, the spindle has to be moved in a controlled manner within the dividing cell. It seems likely that changes in local regions of the cell cortex direct such spindle movements and that motor proteins localized there pull one of the spindle poles, via its astral microtubules, to the appropriate region. Genetic analyses in C. elegans and Drosophila have identified some of the proteins required for such asymmetric divisions, and some of these proteins seem to have a similar role in vertebrates.
Although nuclear division is usually followed by cytoplasmic division, there are exceptions. Some cells undergo multiple rounds of nuclear division without intervening cytoplasmic division. In the early Drosophila embryo, for example, the first 13 rounds of nuclear division occur without cytoplasmic division, resulting in the formation of a single large cell containing several thousand nuclei, arranged in a monolayer near the surface. A cell in which multiple nuclei share the same cytoplasm is called a syncytium. This arrangement greatly speeds up early development, as the cells do not have to take the time to go through all the steps of cytokinesis for each division. After these rapid nuclear divisions, membranes are created around each nucleus in one round of coordinated cytokinesis called cellularization. The plasma membrane extends inward and, with the help of an actin– myosin ring, pinches off to enclose each nucleus (Figure 17–51).
Nuclear division without cytokinesis also occurs in some types of mammalian cells. Megakaryocytes, which produce blood platelets, and some hepatocytes and heart muscle cells, for example, become multinucleated in this way.
After cytokinesis, most cells enter G1, in which Cdks are mostly inactive. We end this section by discussing how this state is achieved at the end of M phase.
The g1 phase Is a stable state of Cdk Inactivity
A key regulatory event in late M phase is the inactivation of Cdks, which is driven primarily by APC/C-dependent cyclin destruction. As described earlier, the inactivation of Cdks in late M phase has many functions: it triggers the events of late mitosis, promotes cytokinesis, and enables the synthesis of prereplicative complexes at DNA replication origins. It also provides a mechanism for resetting the