ORCID Profile
0000-0002-7401-8081
Current Organisation
King's College London
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Publisher: Cold Spring Harbor Laboratory
Date: 12-2003
DOI: 10.1101/GR.1362303
Publisher: Cold Spring Harbor Laboratory
Date: 06-01-2021
DOI: 10.1101/2021.01.06.425462
Abstract: Quiescence is a cellular state characterised by reversible cell-cycle arrest and diminished biosynthetic activity that protects against environmental insults, replicative exhaustion and proliferation-induced mutations 1 . Entry into and exit from this state controls development, maintenance and repair of tissues plus, in the adult central nervous system, generation of new neurons and thus cognition and mood 2–4 . Cancer stem cells too can undergo quiescence, which confers them resistance to current therapies 5, 6 . Despite clinical relevance, quiescence is poorly understood and is defined functionally given lack of molecular markers. Decrease of the most resource-intensive cellular process of protein synthesis is a feature of quiescence, controlled across species and cell types by inhibition of the Target of Rapamycin (TOR) pathway 1, 7 . Here, we combine Drosophila genetics and a mammalian model to show that altered nucleocytoplasmic partitioning and nuclear accumulation of polyadenylated RNAs are novel evolutionarily conserved hallmarks of quiescence regulation. Furthermore, nuclear accumulation of messenger RNA (mRNA) in quiescent NSCs (qNSCs) largely predicts protein downregulation, accounting for uncoupling between transcriptome and proteome in quiescence. These mechanisms provide a previously unappreciated regulatory layer to reducing protein synthesis in quiescent cells, whilst priming them for reactivation in response to appropriate cues.
Publisher: Elsevier BV
Date: 02-2010
DOI: 10.1016/J.CONB.2009.12.005
Abstract: Neural stem and progenitor cells generate the central nervous system (CNS) in organisms as erse as insects and mammals. In Drosophila, multipotent asymmetrically iding progenitors called neuroblasts produce neurons and glia throughout the developing CNS. Nevertheless, the time-windows of mitotic activity, the ision modes, the termination mechanisms and the lineage sizes of in idual neuroblasts all vary considerably from region-to-region. Recent studies shed light on some of the mechanisms underlying this neuroblast ersity and, in particular, how proliferation is boosted in two brain regions. In the central brain, some specialised neuroblasts generate intermediate neural progenitors that can each ide multiple times, thus increasing overall lineage size. In the optic lobe, an alternative expansion strategy involves symmetrically iding neuroepithelial cells generating large numbers of asymmetrically iding neuroblasts. Evidence is also emerging for a cell-intrinsic timer that alters the properties of each neuroblast with increasing developmental age. The core mechanism corresponds to a series of transcription factors that coordinates temporal changes in neuronal/glial identity with transitions in neuroblast cell-cycle speed, entry into quiescence and, ultimately, with termination.
Publisher: EMBO
Date: 04-05-2018
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Rita Sousa-Nunes.