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Titolo:
RAPAMYCIN INDUCES THE G(0) PROGRAM OF TRANSCRIPTIONAL REPRESSION IN YEAST BY INTERFERING WITH THE TOR SIGNALING PATHWAY
Autore:
ZARAGOZA D; GHAVIDEL A; HEITMAN J; SCHULTZ MC;
Indirizzi:
UNIV ALBERTA,DEPT BIOCHEM EDMONTON AB T6G 2H7 CANADA UNIV ALBERTA,DEPT BIOCHEM EDMONTON AB T6G 2H7 CANADA DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT GENET DURHAM NC 27710 DUKE UNIV,MED CTR,HOWARD HUGHES MED INST,DEPT PHARMACOL DURHAM NC 27710
Titolo Testata:
Molecular and cellular biology
fascicolo: 8, volume: 18, anno: 1998,
pagine: 4463 - 4470
SICI:
0270-7306(1998)18:8<4463:RITGPO>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
RNA-POLYMERASE-III; CASEIN KINASE-II; TATA-BINDING PROTEIN; SACCHAROMYCES-CEREVISIAE; STATIONARY-PHASE; FK506-BINDING PROTEIN; GENE-TRANSCRIPTION; REGULATORY SUBUNIT; CELL; CYCLE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
D. Zaragoza et al., "RAPAMYCIN INDUCES THE G(0) PROGRAM OF TRANSCRIPTIONAL REPRESSION IN YEAST BY INTERFERING WITH THE TOR SIGNALING PATHWAY", Molecular and cellular biology, 18(8), 1998, pp. 4463-4470

Abstract

The macrolide antibiotic rapamycin inhibits cellular proliferation byinterfering with the highly conserved TOR (for target of rapamycin) signaling pathway. Growth arrest of budding yeast cells treated with rapamycin is followed by the program of molecular events that characterizes entry into G(0) (stationary phase), including the induction of polymerase (Pol) II genes typically expressed only in G(0). Normally, progression into G(0) is characterized by transcriptional repression of the Pol I and III genes. Here, we show that rapamycin treatment also causes the transcriptional repression of Pol I and III genes. The down-regulation of Pol III transcription is TOR dependent. While it coincides,vith translational repression by rapamycin, transcriptional repression is due in part to a translation-independent effect that is evident in extracts from a conditional tor2 mutant. Biochemical experiments reveal that RNA Pol III and probably transcription initiation factor TFIIIB are targets of repression by rapamycin. In view of previous evidence that TFIIIB and Pol III are inhibited when protein phosphatase 2A (PP2A) function is impaired, and that PP2A is a component of the TOR pathway, our results suggest that TOR signaling regulates Pol I and Pol III transcription in response to nutrient growth signals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 10:22:23