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Title

Primate-specific RFPL1 gene controls cell-cycle progression through cyclin B1/Cdc2 degradation

Authors
Laforge, T
Dehay, C
Published in Cell Death and Differentiation. 2011, vol. 18, no. 2, p. 293-303
Abstract Ret finger protein-like 1 (RFPL1) is a primate-specific target gene of Pax6, a key transcription factor for pancreas, eye and neocortex development. However, its cellular activity remains elusive. In this article, we report that Pax6-elicited expression of the human (h)RFPL1 gene in HeLa cells can be enhanced by in vivo p53 binding to its promoter and therefore investigated the hypothesis that hRFPL1 regulates cell-cycle progression. Upon expression in these cells, hRFPL1 decreased cell number through a kinase-dependent mechanism as PKC activates and Cdc2 inhibits hRFPL1 activity. hRFPL1 antiproliferative activity led to an increased cell population in G(2)/M phase and specific cyclin B1 and Cdc2 downregulations, which were precluded by a proteasome inhibitor. Specifically, cytoplasm-localized hRFPL1 prevented cyclin B1 and Cdc2 accumulation during interphase. Consequently, cells showed a delayed entry into mitosis and cell-cycle lengthening resulting from a threefold increase in G(2) phase duration. Given previous reports that RFPL1 is expressed during cell differentiation, its impact on cell-cycle lengthening therefore provides novel insights into primate-specific development.
Keywords AnimalsCarrier Proteins/genetics/metabolism/physiologyCell DivisionCyclin B/metabolismCyclin B1/metabolismEye Proteins/metabolismG2 PhaseHeLa CellsHomeodomain Proteins/metabolismHumansInterphaseMitosisPaired Box Transcription Factors/metabolismPrimates/metabolismPromoter Regions, GeneticProtein BindingProtein Kinase C/metabolismRepressor Proteins/metabolismTumor Suppressor Protein p53/metabolism
Identifiers
PMID: 20725088
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Structures
Research group Radicaux libres et cellules souches embryonnaires (60)
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BONNEFONT, Jérôme et al. Primate-specific RFPL1 gene controls cell-cycle progression through cyclin B1/Cdc2 degradation. In: Cell Death and Differentiation, 2011, vol. 18, n° 2, p. 293-303. https://archive-ouverte.unige.ch/unige:25091

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Deposited on : 2013-01-08

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