| Abstract: |
A chimeric plasmid, (−1,500)hαCAT, containing approximately 1,500 bp of 5′-flanking DNA of the human glycoprotein hormone α-subunil gene directing the expression of the bacterial chloramphenicol acetyl transferase (CAT) gene, was transfected transiently into rat pituitary-derived GH3 cells. (−1,500)hαCAT expression was stimulated 5- to 20-fold by dexamethasone and 3- to 5-fold by 8-bromo-cAMP (8-Br-cAMP), and was inhibited by 50% by L-triiodothyronine (T3). Thus, suppression by T3 in this system was similar to that seen in pituitary thyrotropes. Induction of (−1,500)hαCAT expression by dexamethasone was antagonized by T3 but was unaffected by 8-Br-cAMP. However, T3 augmented the stimulation of (−1,500)hαCAT activity by 8-Br-cAMP. Deletants containing less than 346 bp of 5′-flanking αDNA showed a stepwise decrease in induction by dexamethasone, suggesting that multiple sequence elements located in this region are required for full induction of hαCAT activity. Deletion analysis also indicated that a thyroid hormone response element is located between 207 and 172 bp of the α gene transcriptional start site. Our finding of induction of α expression by dexamethasone in pituitary cells contrasts with the inhibition of α gene activity by glucocorticoids which has previously been shown in placental cells. Therefore, these data indicate that cell-type-specific factors play an important role in the modulation of α gene transcription. © 1989, Mary Ann Liebert, Inc. All rights reserved. |
| Keywords: |
human cell; animal; cell line; dexamethasone; transcription, genetic; transfection; rna; gene expression regulation; dna; plasmids; rats; radioisotope; chromosome deletion; glycoprotein; liothyronine; hypophysis; triiodothyronine; pituitary neoplasms; human; chloramphenicol acetyltransferase; chloramphenicol o-acetyltransferase; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; genes, structural; 8 bromo cyclic amp; glycoprotein hormones, alpha subunit
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