2,3,7,8-Tetrachlorodibenzo-p-dioxin receptors in wild type and variant mouse hepatoma cells. Nuclear location and strength of nuclear binding.
The volume of aqueous solvent present during subcellular fractionation of mouse hepatoma (Hepa 1c1c7) cells influences the distribution of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) receptors between the nuclear and cytosolic fractions. When the effects of dilution are minimized, at least 80% of the receptors associate with nuclei. The receptors bind relatively strongly to nuclei, as measured by their release by KCl. TCDD-receptor complexes bind more strongly to nuclei than do unoccupied receptors. A temperature-dependent event further enhances the binding of TCDD-receptor complexes to nuclei. A class of variant cells contains receptors which bind relatively weakly to nuclei; this defect accounts for the variant phenotype. We conclude that, in the intact cell, TCDD receptors are located within the nucleus and that the temperature-dependent event in the induction of cytochrome P1-450 gene expression is one which strengthens the binding of the TCDD-receptor complex to chromatin.
D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D008114:Liver Neoplasms, Experimental / Q000378:metabolism*; D051379:Mice; D000072317:Polychlorinated Dibenzodioxins / Q000378:metabolism; D011189:Potassium Chloride / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon; D011955:Receptors, Drug / Q000378:metabolism*; D013696:Temperature
D000072317:Polychlorinated Dibenzodioxins; D018336:Receptors, Aryl Hydrocarbon; D011955:Receptors, Drug; D011189:Potassium Chloride