Nucleic Acids Research, Vol 27, Issue 9 2022-2028, Copyright © 1999 by Oxford University Press
JF Flanagan and CL Peterson
The yeast SWI/SNF complex is required for expression of many genes and for
the 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 a binding 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 both
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.
ARTICLES
A role for the yeast SWI/SNF complex in DNA replication
Program in Molecular Medicine and Department of Biochemistry and Molecular Biology, University of Massachusetts Medical Center, Worcester, MA 01605, USA.
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