Inducible changes in cell size and attachment area due to expression of a mutant SWI/SNF chromatin remodeling enzyme
Hill, David A. ; Chiosea, Simion I. ; Jamaluddin, Saha ; Roy, Kanaklata ; Fischer, Andrew H ; Boyd, Douglas D. ; Nickerson, Jeffrey A. ; Imbalzano, Anthony N.
Citations
Authors
Chiosea, Simion I.
Jamaluddin, Saha
Roy, Kanaklata
Fischer, Andrew H
Boyd, Douglas D.
Nickerson, Jeffrey A.
Imbalzano, Anthony N.
Student Authors
Faculty Advisor
Academic Program
UMass Chan Affiliations
Document Type
Publication Date
Keywords
Adenosine Triphosphatases
Adenosine Triphosphate
Animals
Blotting, Northern
Blotting, Western
Cell Adhesion
Cell Differentiation
Cell Line
Cell Line, Tumor
Cell Nucleus
Cell Size
Chromatin
Collagen
Cytoskeletal Proteins
Cytoskeleton
DNA Helicases
DNA, Complementary
Dose-Response Relationship, Drug
Drug Combinations
Focal Adhesions
Gene Expression Regulation
Heterozygote
Humans
Laminin
Mice
Mutation
Neoplasm Metastasis
Nuclear Proteins
Paxillin
Phosphoproteins
Protein Binding
Protein Structure, Tertiary
Proteoglycans
RNA, Messenger
Receptors, Cell Surface
Time Factors
Transcription Factors
Cell Biology
Life Sciences
Medicine and Health Sciences
Subject Area
Embargo Expiration Date
Link to Full Text
Abstract
The SWI/SNF enzymes belong to a family of ATP-dependent chromatin remodeling enzymes that have been functionally implicated in gene regulation, development, differentiation and oncogenesis. BRG1, the catalytic core subunit of some of the SWI/SNF enzymes, can interact with known tumor suppressor proteins and can act as a tumor suppressor itself. We report that cells that inducibly express ATPase-deficient versions of BRG1 increase in cell volume, area of attachment and nuclear size upon expression of the mutant BRG1 protein. Examination of focal adhesions reveals qualitative changes in paxillin distribution but no difference in the actin cytoskeletal structure. Increases in cell size and shape correlate with over-expression of two integrins and the urokinase-type plasminogen activator receptor (uPAR), which is also involved in cell adhesion and is often over-expressed in metastatic cancer cells. These findings demonstrate that gene expression pathways affected by chromatin remodeling enzymes can regulate the physical dimensions of mammalian cell morphology.
Source
J Cell Sci. 2004 Nov 15;117(Pt 24):5847-54. Link to article on publisher's site