Analysis of Ah gene locus by somatic cell hybridization: expression of Ah regulatory gene product for 2,3,7,8,-tetrachlorodibenzo-p-dioxin in mouse L-cell x mouse hepatoma cell hybrids.
Properties of the aryl hydrocarbon hydroxylase (AHH) enzyme system were examined in polycyclic aromatic hydrocarbon (PAH) -noninducible L-cell x PAH-inducible hepatoma (Hepa) mouse cell hybrids. In hybrids, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces AHH activity. The levels of maximal TCDD-induced AHH activity in the hybrids and the Hepa parent are similar, although a greater concentration of TCDD is required for expression in the hybrids. This concentration difference appears to reflect dilution of AHH-associated gene products by the L-cell parent rather than altered gene expression. The regulatory gene product, the Ah receptor, is expressed similarly in the hybrids and Hepa parent. Both demonstrate specific, high-affinity binding of [3H]TCDD to an equivalent number of receptor sites per cell. These results suggest that the molecular mechanism of phenotypic resemblance to the inducible Hepa parent (i.e., "dominance") in the mouse L-cell x Hepa hybrids involves expression of only the Hepa Ah gene complex.