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Titolo:
A role for the yeast SWI/SNF complex in DNA replication
Autore:
Flanagan, JF; Peterson, CL;
Indirizzi:
Univ Massachusetts, Med Ctr, Program Mol Med, Worcester, MA 01605 USA UnivMassachusetts Worcester MA USA 01605 ol Med, Worcester, MA 01605 USA UnivSAassachusetts, Med Ctr, Dept Biochem & Mol Biol, Worcester, MA 01605 U Univ Massachusetts Worcester MA USA 01605 Mol Biol, Worcester, MA 01605 U
Titolo Testata:
NUCLEIC ACIDS RESEARCH
fascicolo: 9, volume: 27, anno: 1999,
pagine: 2022 - 2028
SICI:
0305-1048(19990501)27:9<2022:ARFTYS>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
UPSTREAM ACTIVATING SEQUENCE; SWI-SNF COMPLEX; SACCHAROMYCES-CEREVISIAE; FUNCTIONAL-ANALYSIS; TRANSCRIPTIONAL ACTIVATORS; BINDING SITE; IN-VIVO; ORIGIN; RECOGNITION; ELEMENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Peterson, CL UniveMassachusetts, Med Ctr, Program Mol Med, 373 Plantat St,Biotech 2,Suit Univ Massachusetts 373 Plantat St,Biotech 2,Suite 301 Worcester MA USA 01605
Citazione:
J.F. Flanagan e C.L. Peterson, "A role for the yeast SWI/SNF complex in DNA replication", NUCL ACID R, 27(9), 1999, pp. 2022-2028

Abstract

The yeast SWI/SNF complex is required for expression of many genes and forthe-full functioning of several transcriptional activators. Genetic and biochemical studies indicate that SWI/SNF uses the energy of ATP hydrolysis to antagonize chromatin-mediated transcriptional repression. We have tested the possibility that SWI/SNF might also play a role in DNA replication. A mitotic minichromosome stability assay was used to investigate the replication efficiency of a variety of autonomous replication sequences (ARSs) in the. presence and absence of SWI/SNF. The stability of minichromosomes that contain ARS1, ARS309 or ARS307 is not altered by lack of SWI/SNF, whereas the functioning of ARS121 is crippled when SWI/SNF is inactivated. The SWI/SNF dependence of ARS121 does not require the replication:enhancer factor, ABF1, and thus, it appears to be a property of a minimal ARS121 origin. Likewise, a minimal derivative of ARS1 that lacks the ABF1 replication enhancer acquires SWI/SNF dependence. Replacing the ABF1 binding site at ARS1 with abinding site for the LexA-GAL4 chimeric activator also creates a SWI/SNF-dependent ARS. Our studies suggest that the SWI/SNF chromatin remodeling complex can play a role in bath replication and transcription and, furthermore; that SWI/SNF dependence of ARS elements is a property of both an ARS-specific replication enhancer and the overall organization of ARS sequence elements.

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Documento generato il 23/01/21 alle ore 09:22:13