Retinoic acid-induced changes in differentiation-defective embryonal carcinoma RAC65 cells.
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 alpha (RAR alpha) which, however, does not fully explain their defect. Here we show that RAC65 cells exhibit an additional defect in RAR alpha 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 defect in RAC65 RAR alpha results in reduced expression of the CRABP gene after RA treatment and, therefore, increased flow of RA into the nucleus.
Malý
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P
Institute of Molecular Genetics, Czechoslovak Academy of Sciences, Prague.
Dráber
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P
D000818:Animals; D002352:Carrier Proteins / Q000235:genetics*; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism; D054278:Embryonal Carcinoma Stem Cells; D000939:Epitopes / Q000032:analysis; D015870:Gene Expression / Q000187:drug effects; D051379:Mice; D014411:Neoplastic Stem Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018168:Receptors, Retinoic Acid; D012045:Regulatory Sequences, Nucleic Acid; D014212:Tretinoin / Q000378:metabolism / Q000494:pharmacology*
D002352:Carrier Proteins; D000939:Epitopes; D012333:RNA, Messenger; D018168:Receptors, Retinoic Acid; D014212:Tretinoin