Please use this identifier to cite or link to this item: https://doi.org/10.1101/gad.1487506
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dc.titleAurora-A acts as a tumor suppressor and regulates self-renewal of Drosophila neuroblasts
dc.contributor.authorWang, H.
dc.contributor.authorSomers, G.W.
dc.contributor.authorBashirullah, A.
dc.contributor.authorHeberlein, U.
dc.contributor.authorYu, F.
dc.contributor.authorChia, W.
dc.date.accessioned2014-05-19T02:50:18Z
dc.date.available2014-05-19T02:50:18Z
dc.date.issued2006-12-15
dc.identifier.citationWang, 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
dc.identifier.issn08909369
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/52805
dc.description.abstractThe 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.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1101/gad.1487506
dc.sourceScopus
dc.subjectAsymmetric division
dc.subjectNeuroblast
dc.subjectSelf-renewal
dc.subjectStem cells
dc.subjectTumor suppressor
dc.typeArticle
dc.contributor.departmentDEAN'S OFFICE (MEDICINE)
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1101/gad.1487506
dc.description.sourcetitleGenes and Development
dc.description.volume20
dc.description.issue24
dc.description.page3453-3463
dc.description.codenGEDEE
dc.identifier.isiut000242996100011
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