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Activation and partial proteolysis of variant glucocorticoid receptors, studied by two-phase partitioning

Insights

Glucocorticoid receptor variants with altered DNA affinity were studied. Only high-affinity variants showed changes in surface properties, suggesting altered receptor charge affects DNA binding in resistant lymphoma cells.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Glucocorticoid resistance in mouse lymphoma cells is often linked to altered glucocorticoid receptor (GR) affinity for nuclei and DNA.
  • Receptor variants include those with abnormally low (nt-) or high (nti) affinity for DNA.

Purpose of the Study:

  • To investigate if abnormal DNA affinities of GR variants correlate with changes in receptor charge and surface properties.
  • To assess these properties using partition coefficients in aqueous two-phase systems.

Main Methods:

  • Utilized cultured mouse lymphoma cell lines with glucocorticoid resistance.
  • Employed aqueous dextran/poly(ethylene glycol) two-phase systems to determine receptor partition coefficients.
  • Performed partial proteolysis using alpha-chymotrypsin and trypsin on wild-type and variant receptors.
  • Assessed DNA and dextran sulfate binding affinities of treated and untreated receptors.

Main Results:

  • No GR variant showed defects in the activation step.
  • Only nti (high-affinity) receptors exhibited abnormal partition properties, indicating altered surface characteristics.
  • Partial proteolysis of wild-type and nt- receptors with alpha-chymotrypsin yielded forms with partition properties similar to nti receptors.
  • Alpha-chymotrypsin treatment normalized DNA-binding properties of wild-type receptors to match nti receptors, while nt- receptors remained less bound.
  • Proteolysis increased dextran sulfate binding, but this varied less between receptor types than DNA affinity.
  • Trypsin treatment abolished DNA and dextran sulfate binding.

Conclusions:

  • Abnormal DNA binding affinities in glucocorticoid-resistant lymphoma cells are associated with altered receptor surface properties, particularly in high-affinity variants.
  • Proteolytic modification can mimic the altered surface and DNA-binding characteristics of nti receptors.
  • Receptor charge and surface properties, as revealed by partition coefficients, play a role in DNA interaction and may contribute to glucocorticoid resistance mechanisms.

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