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Changes in Chromatin Accessibility Across the GM-CSF Promoter upon T Cell Activation Are Dependent on Nuclear Factor B Proteins

Division of Molecular Bioscience, John Curtin School of Medical Research, Australian National University, ACT 2601, Australia

Address correspondence to M. Frances Shannon, Division of Molecular Bioscience, John Curtin School of Medical Research, P.O. Box 334, Canberra ACT 2601, Australia. Phone: 61-(0)2-61259690; Fax: 61-(0)2-61250415; E-mail: frances.shannon{at}anu.edu.au

Granulocyte/macrophage colony-stimulating factor (GM-CSF) is a key cytokine in myelopoiesis and aberrant expression is associated with chronic inflammatory disease and myeloid leukemias. This aberrant expression is often associated with constitutive nuclear factor (NF)-B activation. To investigate the relationship between NF-B and GM-CSF transcription in a chromatin context, we analyzed the chromatin structure of the GM-CSF gene in T cells and the role of NF-B proteins in chromatin remodeling. We show here that chromatin remodeling occurs across a region of the GM-CSF gene between -174 and +24 upon T cell activation, suggesting that remodeling is limited to a single nucleosome encompassing the proximal promoter. Nuclear NF-B levels appear to play a critical role in this process. In addition, using an immobilized template assay we found that the ATPase component of the SWI/SNF chromatin remodeling complex, brg1, is recruited to the GM-CSF proximal promoter in an NF-B–dependent manner in vitro. These results suggest that chromatin remodeling across the GM-CSF promoter in T cells is a result of recruitment of SWI/SNF type remodeling complexes by NF-B proteins binding to the CD28 response region of the promoter.

Key Words: transcription • chromatin remodeling • Brg1 • cytokine • RelA

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