Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pbio.1001494
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dc.titleHedgehog Signaling Acts with the Temporal Cascade to Promote Neuroblast Cell Cycle Exit
dc.contributor.authorChai, P.C.
dc.contributor.authorLiu, Z.
dc.contributor.authorChia, W.
dc.contributor.authorCai, Y.
dc.date.accessioned2014-12-01T06:55:09Z
dc.date.available2014-12-01T06:55:09Z
dc.date.issued2013
dc.identifier.citationChai, P.C., Liu, Z., Chia, W., Cai, Y. (2013). Hedgehog Signaling Acts with the Temporal Cascade to Promote Neuroblast Cell Cycle Exit. PLoS Biology 11 (2) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pbio.1001494
dc.identifier.issn15449173
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/113497
dc.description.abstractIn Drosophila postembryonic neuroblasts, transition in gene expression programs of a cascade of transcription factors (also known as the temporal series) acts together with the asymmetric division machinery to generate diverse neurons with distinct identities and regulate the end of neuroblast proliferation. However, the underlying mechanism of how this "temporal series" acts during development remains unclear. Here, we show that Hh signaling in the postembryonic brain is temporally regulated; excess (earlier onset of) Hh signaling causes premature neuroblast cell cycle exit and under-proliferation, whereas loss of Hh signaling causes delayed cell cycle exit and excess proliferation. Moreover, the Hh pathway functions downstream of Castor but upstream of Grainyhead, two components of the temporal series, to schedule neuroblast cell cycle exit. Interestingly, hh is likely a target of Castor. Hence, Hh signaling provides a link between the temporal series and the asymmetric division machinery in scheduling the end of neurogenesis. © 2013 Chai et al.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1371/journal.pbio.1001494
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.contributor.departmentDEAN'S OFFICE (MEDICINE)
dc.description.doi10.1371/journal.pbio.1001494
dc.description.sourcetitlePLoS Biology
dc.description.volume11
dc.description.issue2
dc.description.page-
dc.description.codenPBLIB
dc.identifier.isiut000315355500018
dc.published.statePublished
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