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|Title:||Aurora-A acts as a tumor suppressor and regulates self-renewal of Drosophila neuroblasts||Authors:||Wang, H.
|Issue Date:||15-Dec-2006||Citation:||Wang, H., Somers, G.W., Bashirullah, A., Heberlein, U., Yu, F., Chia, W. (2006-12-15). Aurora-A acts as a tumor suppressor and regulates self-renewal of Drosophila neuroblasts. Genes and Development 20 (24) : 3453-3463. ScholarBank@NUS Repository. https://doi.org/10.1101/gad.1487506||Abstract:||The choice of self-renewal versus differentiation is a fundamental issue in stem cell and cancer biology. Neural progenitors of the Drosophila post-embryonic brain, larval neuroblasts (NBs), divide asymmetrically in a stem cell-like fashion to generate a self-renewing NB and a Ganglion Mother Cell (GMC), which divides terminally to produce two differentiating neuronal/glial daughters. Here we show that Aurora-A (AurA) acts as a tumor suppressor by suppressing NB self-renewal and promoting neuronal differentiation. In aurA loss-of-function mutants, supernumerary NBs are produced at the expense of neurons. AurA suppresses tumor formation by asymmetrically localizing atypical protein kinase C (aPKC), an NB proliferation factor. Numb, which also acts as a tumor suppressor in larval brains, is a major downstream target of AurA and aPKC. Notch activity is up-regulated in aurA and numb larval brains, and Notch signaling is necessary and sufficient to promote NB self-renewal and suppress differentiation in larval brains. Our data suggest that AurA, aPKC, Numb, and Notch function in a pathway that involved a series of negative genetic interactions. We have identified a novel mechanism for controlling the balance between self-renewal and neuronal differentiation during the asymmetric division of Drosophila larval NBs. © 2006 by Cold Spring Harbor Laboratory Press.||Source Title:||Genes and Development||URI:||http://scholarbank.nus.edu.sg/handle/10635/52805||ISSN:||08909369||DOI:||10.1101/gad.1487506|
|Appears in Collections:||Staff Publications|
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