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Kinetic Complexity of the Global Response to Glucocorticoid Receptor Action

Laboratory of Receptor Biology and Gene Expression (S.J., T.A.J., M.-H.S., S.C.B., C.A.K.-P., G.L.H.), National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-5055; Henry Wellcome Labs for Integrative Neuroscience, and Endocrinology (S.C.B.), University of Bristol, Bristol BS1 3NY, United Kingdom; Helmholtz Center for Environmental Research-Umweltforschungszentrum (S.T.), Department of Environmental Immunology, D-04318 Leipzig, Germany; and Genetics Branch (S.R.D., R.W., P.S.M.), National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892

Address all correspondence and requests for reprints to: Gordon L. Hager, Laboratory of Receptor Biology and Gene Expression, Building 41, Room B602, 41 Library Drive, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-5055. E-mail: hagerg{at}exchange.nih.gov.

We have characterized the kinetic response of gene targets throughout the murine genome to transcriptional modulation by the glucocorticoid receptor (GR). In contrast to a model in which multiple genes are either repressed or activated during the GR response, the vast majority of responsive genes are subject to complex regulation profiles, frequently with alternate activation and repression phases. We also observe that GR binding at response elements does not always correlate with the target gene response profile. Thus, the cellular response to GR stimulation involves a highly orchestrated series of regulatory actions and not simply a binary response to hormone.