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Transient expression experiments, using chimeric plasmids containing 3000 base pairs of PRL 5'-flanking sequences linked to the bacterial chloramphenicol acetyl transferase structural gene, demonstrate that L-T3 can inhibit (GH1 cells) or stimulate (GH4C1 cells) chloramphenicol acetyl transferase activity. Deletion experiments have defined the region necessary for these effects to sequences between -176 and -11 of the PRL gene. This region seems to contain the sequences necessary both for basal expression and for L-T3 regulation. Gel mobility shift experiments revealed that proteins extracted from GH1 and GH4C1 cell nuclei but not rat-2 fibroblasts interact with the PRL gene from -176 to +75. DNase I footprinting studies reveal two footprints which are the same in all pituitary derived cells tested. These footprints are not seen in rat-2 fibroblasts. Neither of these footprints likely represents binding of the L-T3-receptor since extracts from cells containing very low levels of receptor form footprints identical to those from cells with an abundance of receptors. These results suggest that different trans-acting factors, not identifiable by conventional footprinting techniques, are present in these cell lines which account for their opposite responses to L-T3. The regulation of PRL gene expression by L-T3 is unique in that both stimulation and suppression can be demonstrated using a single hormone-gene system. This should allow us to answer fundamental questions regarding the molecular switch between stimulation and suppression of gene expression by hormones.

Transcriptional Regulation of Prolactin Gene Expression by Thyroid Hormone—Alternate Suppression and Stimulation in Different GH Cell Lines