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Mouse Cellular Retinoic Acid Binding Protein: Cloning, Complementary DNA Sequence, and Messenger RNA Expression during the Retinoic Acid-induced Differentiation of F9 Wild Type and Ra-3-10 Mutant Teratocarcinoma Cells¹

Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, and Division of Cell and Molecular Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115

Retinoic acid, a natural derivative of vitamin A (retinol), induces mouse F9 teratocarcinoma stem cells to differentiate into nontumorigenic parietal endoderm cells. The mouse cellular retinoic acid binding protein (CRABP) has been implicated in the mechanism of action of retinoic acid (RA), since a mutant F9 cell line, RA-3-10, which possesses less than 5% of the wild type level of [³H]RA:CRABP binding activity, fails to differentiate in response to RA. In order to study the CRABP in this RA-induced differentiation process, we have cloned and sequenced the full-length mouse CRABP complementary DNA and have characterized its expression in wild type F9 and mutant cells. The mouse CRABP mRNA is a single, low abundant mRNA approximately 800 bases in length. The steady state level of the CRABP mRNA was measured in untreated stem cells and after the addition of RA alone, dibutyryl cyclic AMP plus theophylline (CT), or retinoic acid, dibutyryl cyclic AMP and theophylline (RACT) to F9 wild type and the mutant RA-3-10 cells. The CRABP mRNA was present in wild type F9 stem cells, and the level of its expression was changed by RA. When RA was added to F9 wild type cells, the steady state level of CRABP mRNA decreased 2- to 3-fold. When RACT was added to wild type cells, the level of CRABP mRNA increased and then decreased, resulting in a peak of CRABP mRNA expression between 24 and 48 h.

In contrast, untreated mutant RA-3-10 cells had a lower level of CRABP mRNA than wild type stem cells, and the mutant cells responded quite differently to the addition of RA and RACT. The addition of RA caused an impressive 60-fold increase in the steady state level of CRABP mRNA in RA-3-10 cells by 120 h. One interpretation of this result is that there is negative regulation of CRABP mRNA expression, mediated directly or indirectly by the wild type functional CRABP protein, and that this regulation is aberrant in the RA-3-10 cells.

¹ This research was supported by NIH postdoctoral Fellowship CA07274 to C. M. S., March of Dimes Grant 1-966, and NIH Research Grant R01CA43796.

² Established investigator of the American Heart Association. To whom requests for reprints should be addressed, at Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115.

Received 9/13/88. Revised 12/ 1/88. Accepted 12/12/88.

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