<P> Further experimentation with GFP - tagged proteins and mutant proteins indicates that the medial cortical nodes are formed by the ordered, Cdr2 - dependent assembly of multiple interacting proteins during interphase . Cdr2 is at the top of this hierarchy and works upstream of Cdr1 and Blt1 . Mitosis is promoted by the negative regulation of Wee1 by Cdr2 . It has also been shown that Cdr2 recruits Wee1 to the medial cortical node . The mechanism of this recruitment has yet to be discovered . A Cdr2 kinase mutant, which is able to localize properly despite a loss of function in phosphorylation, disrupts the recruitment of Wee1 to the medial cortex and delays entry into mitosis . Thus, Wee1 localizes with its inhibitory network, which demonstrates that mitosis is controlled through Cdr2 - dependent negative regulation of Wee1 at the medial cortical nodes . </P> <P> Cell polarity factors positioned at the cell tips provide spatial cues to limit Cdr2 distribution to the cell middle . In fission yeast Schizosaccharomyces pombe (S. Pombe), cells divide at a defined, reproducible size during mitosis because of the regulated activity of Cdk1 . The cell polarity protein kinase Pom1, a member of the dual - specificity tyrosine - phosphorylation regulated kinase (DYRK) family of kinases, localizes to cell ends . In Pom1 knockout cells, Cdr2 was no longer restricted to the cell middle, but was seen diffusely through half of the cell . From this data it becomes apparent that Pom1 provides inhibitory signals that confine Cdr2 to the middle of the cell . It has been further shown that Pom1 - dependent signals lead to the phosphorylation of Cdr2 . Pom1 knockout cells were also shown to divide at a smaller size than wild - type, which indicates a premature entry into mitosis . </P> <P> Pom1 forms polar gradients that peak at cell ends, which shows a direct link between size control factors and a specific physical location in the cell . As a cell grows in size, a gradient in Pom1 grows . When cells are small, Pom1 is spread diffusely throughout the cell body . As the cell increases in size, Pom1 concentration decreases in the middle and becomes concentrated at cell ends . Small cells in early G2 which contain sufficient levels of Pom1 in the entirety of the cell have inactive Cdr2 and cannot enter mitosis . It is not until the cells grow into late G2, when Pom1 is confined to the cell ends that Cdr2 in the medial cortical nodes is activated and able to start the inhibition of Wee1 . This finding shows how cell size plays a direct role in regulating the start of mitosis . In this model, Pom1 acts as a molecular link between cell growth and mitotic entry through a Cdr2 - Cdr1 - Wee1 - Cdk1 pathway . The Pom1 polar gradient successfully relays information about cell size and geometry to the Cdk1 regulatory system . Through this gradient, the cell ensures it has reached a defined, sufficient size to enter mitosis . </P> <P> Many different types of eukaryotic cells undergo size - dependent transitions during the cell cycle . These transitions are controlled by the cyclin - dependent kinase Cdk1 . Though the proteins that control Cdk1 are well understood, their connection to mechanisms monitoring cell size remains elusive . A postulated model for mammalian size control situates mass as the driving force of the cell cycle . A cell is unable to grow to an abnormally large size because at a certain cell size or cell mass, the S phase is initiated . The S phase starts the sequence of events leading to mitosis and cytokinesis . A cell is unable to get too small because the later cell cycle events, such as S, G2, and M, are delayed until mass increases sufficiently to begin S phase . </P>

Where does cell multiplication takes place in an animal