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ADP-ribosylation of chromosomal proteins and mouse mammary tumor virus gene expression. Glucocorticoids rapidly

Insights

Glucocorticoids rapidly decrease ADP-ribosylation on specific chromosomal proteins (HMG 14 and 17), which is linked to mouse mammary tumor virus gene activation. This suggests a key role for ADP-ribosylation in gene regulation.

Area of Science:

  • Molecular Biology
  • Gene Regulation
  • Cancer Research

Background:

  • Glucocorticoids are key regulators of gene expression.
  • ADP-ribosylation is a post-translational modification involved in various cellular processes.
  • Mouse mammary tumor virus (MMTV) is an oncogenic retrovirus whose expression is influenced by glucocorticoids.

Purpose of the Study:

  • To investigate the relationship between endogenous ADP-ribosylation of chromosomal proteins and glucocorticoid-regulated MMTV gene expression.
  • To determine the specific chromosomal proteins affected by glucocorticoid treatment and their role in MMTV gene expression.

Main Methods:

  • Cultured mouse mammary tumor cells were treated with glucocorticoids.
  • Endogenous ADP-ribosylation levels of various chromosomal proteins, including High Mobility Group (HMG) 14 and 17, were measured.
  • The effect of 3-amino-benzamide, an ADP-ribosylation inhibitor, on MMTV RNA levels was assessed.

Main Results:

  • Glucocorticoids rapidly decreased ADP-ribosylation on HMG 14 and 17 proteins (half-times of 8 and 17 minutes, respectively).
  • ADP-ribosylation on HMG 1 and 2 and histone H1 was less affected by glucocorticoids.
  • 3-Amino-benzamide increased MMTV RNA levels and decreased ADP-ribosylation of HMG 14 and 17.

Conclusions:

  • A decrease in endogenous ADP-ribosylation of HMG 14 and 17 is a direct consequence of glucocorticoid action.
  • The loss of ADP-ribosylation from HMG 14 and 17 proteins may be a critical event in the regulation of mouse mammary tumor virus gene expression.

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