A Novel Basal Promoter Element is Required for Expression of the Rat Tyrosine Hydroxylase Gene

Overview

Journal J Neurosci

Specialty Neurology

Date 1997 Jun 1

PMID 9151724

Citations 6

Authors

S Patankar

M LAZAROFF

S O Yoon

D M Chikaraishi

Affiliations

Soon will be listed here.

Abstract

Transcription of the rat tyrosine hydroxylase (TH) gene is controlled by enhancer sequences in its 5' flanking region; these enhancers include the AP1, dyad, and cAMP response element (CRE) motifs. We show that a novel basal promoter element (-17 GCCTGCCTGGCGA -5) positioned between the TATA box and +1 works in conjunction with the upstream AP1-dyad and CRE enhancers but cannot support transcription by itself. A mutation of this element, termed partial dyad, reduces basal expression of a reporter gene in TH-positive cell lines and TH-negative lines but has no effect on cAMP- or KCl-induced expression. A double mutant at positions -17 and -11 of the partial dyad reduces transcriptional activation by 80%. Conversely, insertion of this element into a heterologous promoter restores basal expression to levels mediated by the native TH promoter. The partial dyad is a novel activational element that is required for full expression of the TH gene and may assist in the function of the AP1, dyad, and CRE motifs and also other enhancers further upstream. Hence, the rat TH gene is unusual in that its enhancers will not function with a heterologous promoter but require a specific TH promoter sequence for full activation.

Citing Articles

Nucleotide sequence conservation of novel and established -regulatory sites within the tyrosine hydroxylase gene promoter.

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Complex molecular regulation of tyrosine hydroxylase.

Tekin I, Roskoski Jr R, Carkaci-Salli N, Vrana K J Neural Transm (Vienna). 2014; 121(12):1451-81.

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A tyrosine hydroxylase-yellow fluorescent protein knock-in reporter system labeling dopaminergic neurons reveals potential regulatory role for the first intron of the rodent tyrosine hydroxylase gene.

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