Cyclin E Associates with BAF155 and BRG1, Components of the Mammalian SWI-SNF Complex, and Alters the Ability of BRG1 To Induce Growth Arrest | Zendy

Fergus Shanahan | Zendy; Wolfgang Seghezzi | Zendy; David Parry | Zendy; Daniel Mahony | Zendy; Emma Lees | Zendy

Open Access

Cyclin E Associates with BAF155 and BRG1, Components of the Mammalian SWI-SNF Complex, and Alters the Ability of BRG1 To Induce Growth Arrest

Author(s) -

Fergus Shanahan,

Wolfgang Seghezzi,

David Parry,

Daniel Mahony,

Emma Lees

Publication year - 1999

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.19.2.1460

Subject(s) - swi/snf , biology , microbiology and biotechnology , cyclin a , chromatin remodeling , chromatin , cyclin d , cyclin a2 , cyclin b , chromatin structure remodeling (rsc) complex , cyclin , cyclin e , cell cycle , cyclin dependent kinase , genetics , cell , gene

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 β-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.

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