Reversible and persistent changes in chromatin structure accompany activation of a glucocorticoid-dependent enhancer element

Cell. 1984 Aug;38(1):29-38. doi: 10.1016/0092-8674(84)90523-3.


A derivative of mouse mammary tumor virus (MTV) DNA, LTL, was constructed in vitro and introduced into the genome of mouse L cells. Transcription of LTL was stimulated by dexamethasone, a glucocorticoid hormone. Two features of LTL chromatin structure are altered upon hormone treatment. First, "moderate" DNAase I sensitivity of the entire LTL element increases following addition of dexamethasone; this alteration persists after hormone withdrawal, when LTL transcription is shut off. Second, a discrete DNAase I-hypersensitive region is induced with a time course that closely parallels the rate of increasing transcription from the MTV promoter; this structure disappears upon hormone removal. The induced hypersensitive region coincides with a segment of the MTV long terminal repeat sequence that specifically binds purified glucocorticoid receptor in vitro and functions as a hormone-dependent enhancer element in vivo. We suggest that specific glucocorticoid receptor-DNA interactions may alter the configuration of DNA or chromatin in the vicinity of the binding sites, thereby creating an active transcriptional enhancer.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Base Sequence
  • Cell Transformation, Neoplastic / drug effects*
  • Chromatin / physiology*
  • DNA Restriction Enzymes
  • Dexamethasone / pharmacology*
  • Genes / drug effects*
  • Genes, Viral / drug effects*
  • L Cells / drug effects
  • L Cells / enzymology
  • Mammary Tumor Virus, Mouse / genetics*
  • Mice
  • Nucleic Acid Hybridization
  • Plasmids
  • Thymidine Kinase / genetics
  • Transcription, Genetic
  • Transfection


  • Chromatin
  • Dexamethasone
  • Thymidine Kinase
  • DNA Restriction Enzymes