Cyclin E Associates with BAF155 and BRG1, Components of the Mammalian SWI-SNF Complex, and Alters the Ability of BRG1 To Induce Growth Arrest
Molecular and Cellular BiologyPublished 1 February 1999Open access
Frances Shanahan, Wolfgang Seghezzi, David Parry, Daniel Mahony, Emma Lees
Citations161
SJR quartileQ2
SJR score0.99
SNIP0.58
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TL;DR
It is suggested that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.
Abstract
SWI-SNF complexes have been implicated in transcriptional regulation by chromatin remodeling. We have identified an interaction between two components of the mammalian SWI-SNF complex and cyclin E, an essential cell cycle regulatory protein required for G1/S transition. BRG1 and BAF155, mammalian homologs of yeast SWI2 and SWI3, respectively, are found in cyclin E complexes and are phosphorylated by cyclin E-associated kinase activity. In this report, we show that overexpression of BRG1 causes growth arrest and induction of senescence-associated beta-galactosidase activity, which can be overcome by cyclin E. Our results suggest that cyclin E may modulate the activity of the SWI-SNF apparatus to maintain the chromatin in a transcriptionally permissive state.
Keywords
Biochemistry, Genetics and Molecular Biology
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