Asymmetric cell divisions can be mediated by the preferential segregation of intrinsic cell fate determinants into one of two sibling daughters. In dividing Drosophila neural progenitors the apical-basal orientation of the mitotic spindle, the basal cortical localization of the cell fate determinants Numb and/or Prospero as well as the coordination of these events are mediated by several proteins which include Bazooka (Baz), Inscuteable (Insc) and Partner of Inscuteable (Pins) which localize as an apical cortical complex starting at interphase. Here I will summarize data which suggest that the formation of this apical complex involves two distinct steps: (1) during the initiation of apical complex formation in interphase neuroblasts, there appears to be a hierarchical relation amongst these components where Baz recruits Insc and Baz/Insc in turn recruit Pins to the apical cortex/stalk; (2) while in delaminated mitotic neuroblasts the maintenance of the apical cortical localization of these proteins is dependent on the presence of all three components. Moreover, we show that the maintenance of this apical protein complex is essential for the correct execution of asymmetric division. Finally, the localization of the various asymmetrically localized proteins shows cell cycle dependence; however, the involvement of the cell cycle regulator in asymmetric cell divisions has not been previously shown. Here we present evidence from ongoing experiments which suggest a requirement for the key cell cycle regulator cdc2 in asymmetric cell divisions.
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