Figure 17–50 An asymmetric cell division segregating cytoplasmic components to only one daughter cell.
These light micrographs illustrate the controlled asymmetric segregation  of specific cytoplasmic components to one daughter cell during the first division of a fertilized egg of the nematode
C. elegans. The fertilized egg is shown in the left micrographs and the two daughter cells in the right micrographs. The cells above have been stained with a blue, dna-binding, fluorescent dye to show the nucleus (and polar bodies); they are viewed by both differential-interference-contrast and fluorescence microscopy. The cells below are the same cells stained with an antibody against p-granules and viewed by fluorescence microscopy. These small granules are made of Rna and proteins and determine which cells become germ cells. They are distributed randomly throughout the cytoplasm of the unfertilized egg (not shown) but become segregated to the posterior pole of the fertilized egg. The cleavage plane is oriented to ensure that only the posterior daughter cell receives  the p-granules when the egg divides. The same segregation process is  repeated in several subsequent cell divisions, so that the p-granules end up only in cells that give rise to eggs and sperm. (Courtesy of susan strome.)
Figure 17–51 Mitosis without cytokinesis in the early Drosophila embryo. (a) The first 13 nuclear divisions occur synchronously and without cytoplasmic division to create a large syncytium. most of the nuclei migrate to the cortex, and the plasma membrane extends inward and pinches off to surround each nucleus to form individual cells in a process called cellularization. (B) Fluorescence micrograph of multiple mitotic spindles in a Drosophila embryo before cellularization. The microtubules are stained green and the centrosomes red. note that all the nuclei go through the cycle synchronously; here, they are all in metaphase, with the unlabeled chromosomes seen as a dark band at the spindle equator. (B, courtesy of kristina Yu and William sullivan.) cell-cycle control system to a state of Cdk inactivity as the cell prepares to enter a new cell cycle. In most cells, this state of Cdk inactivity generates a G1 gap phase, during which the cell grows and monitors its environment before committing to a new cell cycle.
In early animal embryos, the inactivation of M-Cdk in late mitosis is due almost entirely to the action of Cdc20–APC/C, discussed earlier. Recall, however, that M-Cdk stimulates Cdc20–APC/C activity. Thus, the destruction of M-cyclin in late mitosis soon leads to the inactivation of all APC/C activity in an embryonic cell. This APC/C inactivation immediately after mitosis is especially useful in rapid embryonic cell cycles, as it allows the cell to quickly begin accumulating new M-cyclin for the next cycle (Figure 17–52A).
Rapid cyclin accumulation immediately after mitosis is not useful, however, for cells in which a G1 phase is needed to allow control of entry into the next cell cycle. These cells employ several mechanisms to prevent Cdk reactivation after mitosis. One mechanism uses another APC/C-activating protein called Cdh1, mentioned earlier as a close relative of Cdc20 (see Table 17–2). Although both Cdh1 and Cdc20 bind to and activate the APC/C, they differ in one important respect. Whereas M-Cdk activates the Cdc20–APC/C complex, it inhibits the Cdh1–APC/C complex by directly phosphorylating Cdh1. As a result of this relationship, Cdh1– APC/C activity increases in late mitosis after the Cdc20–APC/C complex has initiated the destruction of M-cyclin. M-cyclin destruction therefore continues after mitosis: although Cdc20–APC/C activity has declined, Cdh1–APC/C activity is high (Figure 17–52B).