The regulatory effects of retinoic acid (RA) on retinoic acid receptor (RAR) α,β and γ mRNA were examined in the F9 mouse teratocarcinoma cells. Northern blot hybridization showed that RA regulated all three types of RAR gene expression. The different transcripts for each RAR α and β were differentially regulated by RA. The maximum induction of the 2.8 kb RAR α and 3.3 kb RAR β transcript levels by RA took longer than the induction of the 3.8 kb RAR α and 3.5 kb RAR β transcript levels. The data suggest that these transcripts originated from different promoters. Short term treatment ( ≤ 24 hours) of RA induced both 3.1 and 3.3 kb RAR γ transcripts. Long term treatment (> 24 hours) of RA resulted in the inhibition of 3.1 kb mRNA, whereas the 3.3 kb mRNA remained elevated. In addition, a new RAR γ transcript of 2.9 kb was induced. In contrast to RAR α and β the effect on RAR γ gene expression was irreversible. Cycloheximide did not prevent the effect of RA on RAR gene expression, whereas actinomycin D totally abolished the RA effect on the expression of all three receptor genes. The data suggest that the biological effects of RA may be constrained or augmented by differential regulation of its own receptor gene expression.
|Original language||English (US)|
|Number of pages||6|
|State||Published - 1992|
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Developmental Biology
- Cell Biology