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Título

Balanced production of ribosome components is required for proper G/S transition in saccharomyces cerevisiae

AutorGómez-Herreros, Fernando ; Rodríguez-Galán, Olga ; Morillo-Huesca, Macarena ; Maya, Douglas; Arista-Romero, María; Cruz, Jesús de la; Chávez, Sebastián; Muñoz-Centeno, Mari Cruz
Palabras claveCell Cycle
Ribosomal RNA (rRNA)
Ribosome Assembly
Ribosomes
RNA Polymerase I
RNA Polymerase II
RNA Polymerase III
Transcription
G1/S Transition
Free Ribosomal Proteins
Fecha de publicación16-sep-2013
EditorAmerican Society for Biochemistry and Molecular Biology
CitaciónJournal of Biological Chemistry 288(44): 31689- 31700 (2013)
ResumenCell cycle regulation is a very accurate process that ensures cell viability and the genomic integrity of daughter cells. A fundamental part of this regulation consists in the arrest of the cycle at particular points to ensure the completion of a previous event, to repair cellular damage, or to avoid progression in potentially risky situations. In this work, we demonstrate that a reduction in nucleotide levels or the depletion of RNA polymerase I or III subunits generates a cell cycle delay at the G1/S transition in Saccharomyces cerevisiae. This delay is concomitant with an imbalance between ribosomal RNAs and proteins which, among others, provokes an accumulation of free ribosomal protein L5. Consistently with a direct impact of free L5 on the G1/S transition, rrs1 mutants, which weaken the assembly of L5 and L11 on pre-60S ribosomal particles, enhance both the G1/S delay and the accumulation of free ribosomal protein L5. We propose the existence of a surveillance mechanism that couples the balanced production of yeast ribosomal components and cell cycle progression through the accumulation of free ribosomal proteins. This regulatory pathway resembles the p53-dependent nucleolar-stress checkpoint response described in human cells, which indicates that this is a general control strategy extended throughout eukaryotes. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.
Versión del editorhttp://dx.doi.org/10.1074/jbc.M113.500488
URIhttp://hdl.handle.net/10261/122739
DOI10.1074/jbc.M113.500488
Identificadoresdoi: 10.1074/jbc.M113.500488
issn: 0021-9258
e-issn: 1083-351X
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