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Published on: November 5, 2012
Nucleosome sliding via TBP DNA binding in vivo
1Department of Biochemistry and Molecular Biophysics, Columbia University, 630 West 168th Street, New York, NY 10032, USA.
Cell
|September 27, 2001
Summary
Virus infection causes nucleosomes to slide, exposing key DNA sites for gene activation. This chromatin remodeling involves SWI/SNF and DNA bending, crucial for transcriptional regulation.
Area of Science:
- Molecular Biology
- Epigenetics
- Gene Regulation
Background:
- Nucleosomes can obstruct DNA access for transcription factors.
- IFN-beta promoter activation requires specific DNA elements to be accessible.
Purpose of the Study:
- To investigate the mechanism of nucleosome sliding at the IFN-beta promoter during viral infection.
- To elucidate the role of chromatin remodeling in transcriptional activation.
Main Methods:
- In vivo studies of nucleosome dynamics.
- Analysis of chromatin remodeling complex recruitment (SWI/SNF).
- Investigation of DNA-binding protein interactions and DNA bending.
Main Results:
- Nucleosome sliding in vivo upon viral infection exposes the TATA box and transcription initiation site.
- Chromatin remodeling is a two-step process: SWI/SNF recruitment followed by TBP binding and DNA bending.
- DNA bending capability correlates with nucleosome sliding, suggesting it induces sliding.
Conclusions:
- Nucleosome sliding is a key event in IFN-beta gene activation following viral infection.
- The SWI/SNF complex and DNA bending induced by TBP binding drive nucleosome repositioning.
- This mechanism highlights the dynamic nature of chromatin in regulating gene expression.
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