Affiliation:
1. Stowers Institute for Medical Research, 1000 E 50th St., Kansas City, Missouri 64110
2. Penn State University College
of Medicine, 500 University St., Hershey, Pennsylvania
17033
Abstract
ABSTRACT
SWI/SNF is a well-characterized chromatin remodeling complex that remodels
chromatin by sliding nucleosomes in
cis
and/or displacing
nucleosomes in
trans
. The latter mechanism has the potential
to remove promoter nucleosomes, allowing access to transcription
factors and RNA polymerase. In vivo, histone acetylation often precedes
apparent nucleosome loss; therefore, we sought to determine whether
nucleosomes containing acetylated histones could be displaced by the
SWI/SNF chromatin remodeling complex. We found that SAGA-acetylated
histones were lost from an immobilized nucleosome array when treated
with the SWI/SNF complex. When the nucleosome array was acetylated by
SAGA in the presence of bound transcription activators, it generated a
peak of acetylation surrounding the activator binding sites. Subsequent
SWI/SNF treatment suppressed this acetylation peak. Immunoblots
indicated that SWI/SNF preferentially displaced acetylated histones
from the array relative to total histones. Moreover, the Swi2/Snf2
bromodomain, an acetyl-lysine binding domain, played a role in the
displacement of acetylated histones. These data indicate that targeted
histone acetylation by the SAGA complex predisposes promoter
nucleosomes for displacement by the SWI/SNF
complex.
Publisher
American Society for Microbiology
Subject
Molecular Biology,General Medicine,Microbiology
Cited by
80 articles.
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