RAC65 is a mutant clone of mouse embryonal carcinoma cells, P19, which does not undergo terminal differentiation upon treatment with retinoic acid (RA), RAC65 cells express a truncated RA receptor α (RARα) which, however, does not fully explain their defect. Here we show that RAC65 cells exhibit an additional defect in RARα mRNA which may reflect a defect in RNA splicing. The parental and mutant cells also differ in their capacities to bind [3H]RA into nuclear fractions and in expression of cellular RA binding protein (CRABP) mRNA after treatment with RA. The combined data suggest that the deffect in RAC65 RARα results in reduced expression of the CRABP gene after RA treatment and, therefore, increased flow of RA into the nucleus.
