Uncovering the link between malfunctions in Drosophila neuroblast asymmetric cell division and tumorigenesis

Asymmetric cell division is a phenomenon that has long been studied, especially in the developing nervous system of invertebrates and vertebrates. Asymmetric cell division is a mechanism whereby any given cell divides to give rise to two daughter cells, each of which possesses a different fate than the other [1]. Such “fates” can be manifested as differences in size, morphology, gene expression pattern or the number of subsequent cell divisions undergone by the two newly born daughter cells [1].To date there are two established modes of asymmetric cell division. One type of division, commonly referred to as a niche-controlled, or extrinsic, mechanism of cell division, emphasizes the importance of the stem cell niche (Figure？ 1A) [2]. Environmental factors influence the ability to maintain the progenitor population, and a cell relies on contact with its stem cell niche to be able to self-renew. A second, intrinsic mechanism of asymmetric cell division serves as the dominant mode of division during development and will be the focus of this discussion rather than the niche-controlled mechanism (Figure？ 1B). With regard to the intrinsic mechanism, regulators of self-renewal are asymmetrically localized during mitosis, so that when cells divide only one daughter cell inherits these regulators and thus takes on a different fate than its sister cell [3,4]. Actively dividing Drosophila neuroblasts, which serve as precursor and progenitor cells of the nervous system, take the intrinsic route of asymmetric cell division. A brief background of Drosophila neural progenitor cells will be given in this review. Notch signaling, which is a very important component that ties into the developmental process of neurogenesis, will also be discussed.The major aspects of asymmetric cell division in Drosophila will be discussed at length. An apical-basal axis of polarity is set up within cells, which is used to both asymmetrically distribute self-renewal determinants and orient the mitotic