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The Regulation of Retinoic Acid Receptor mRNA Levels during Spermatogenesis

Program in Genetics and Cell Biology, Washington State University Pullman, Washington 99164
Department of Biochemistry and Biophysics, Washington State University Pullman, Washington 99164

Address requests for reprints to: Kwan Hee Kim, Department of Biochemistry and Biophysics, Washington State University, Pullman, Washington 99164–4660.

Abstract

Retinoic acid receptor- mRNAs were found in both Sertoli and germ cells of the testis. A 2.7-kilobase (kb) mRNA was expressed solely in Sertoli cells, whereas a 3.4-kb mRNA was distributed in both Sertoli and germ cells. In addition, we report two new, but minor, germ cell-specific mRNAs detected primarily in the pachytene spermatocytes. By contrast, only one transcript for retinoic acid receptor-β was found in the testis, exclusively in Sertoli cells. These results suggest that each mRNA may have specific functions in mediating the effects of retinoids during spermatogenesis.

The expression of retinoic acid receptor- mRNAs was regulated during the spermatogenic cycle, showing a 7-fold increase in the level of 3.4-kb mRNA at stages VIII-IX. Since stage VIII is where the development of germ cells is arrested at the prophase of meiosis in the vitamin A-deficient testis, this result suggests that mRNA transcription may be necessary before more advanced germ cells than preleptotene spermatocytes would be observed in the testis.

The most striking finding was that the treatment of vitamin A-deficient rats with retinol led to a rapid increase in the retinoic acid receptor- mRNA levels. The level of mRNAs was increased 3-fold at its peak, but diminished by 12 h. This precise regulation of receptor by retinol suggests that its synthesis is required before it can be used to modulate the transcription of retinoid-inducible genes. In contrast, the regulation of retinoic acid receptor-β mRNA was different from the mRNAs, in that its level remained unchanged for 48 h after the injection of retinol.

FOOTNOTES

This work was supported by NIH Grant HD-25094 (to K.H.K.).

Received for publication July 16, 1990. Revision received August 28, 1990. Accepted for publication August 28, 1990.

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