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pubmed-article:2233709pubmed:abstractTextWe have found that the mouse metallothionein-I (MT-I) gene promoter functions in an unusual, compound manner. It directs both TATA-dependent and TATA-independent modes of transcription in vivo. The TATA-dependent message is initiated at the previously characterized +1 transcription start site and is the predominant species in most tissues. In many cell types it is metal inducible. The TATA-independent initiation sites are distributed over the 160 bp upstream of the previously characterized +1 start site, and the RNA products are present in all tissues examined. Only in testis, however, do the TATA-independent transcripts predominate, accumulating to highest levels in pachytene-stage meiotic cells and early spermatids. Unlike the TATA-dependent +1 transcript, these RNAs are not induced by metal, even in cultured cells in which the +1 species is induced. Transfection studies of site-directed mutants show that destruction of the TATA element drastically alters the ratio of the two RNA classes in cells in which the +1 transcripts normally dominates. In TATA-minus mutants, the TATA-independent RNAs become the most prevalent, although they remain refractory to metal induction. Thus, the MT-I promoter utilizes two different types of core promoter function within a single cell population. The two different types of core promoter respond very differently to environmental stimuli, and the choice between them appears to be regulated in a tissue-specific fashion.lld:pubmed
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pubmed-article:2233709pubmed:authorpubmed-author:GarrettD JDJlld:pubmed
pubmed-article:2233709pubmed:authorpubmed-author:WoldB JBJlld:pubmed
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pubmed-article:2233709pubmed:articleTitleTissue-specific expression from a compound TATA-dependent and TATA-independent promoter.lld:pubmed
pubmed-article:2233709pubmed:affiliationDivision of Biology, California Institute of Technology, Pasadena 91125.lld:pubmed
pubmed-article:2233709pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2233709pubmed:publicationTypeComparative Studylld:pubmed
pubmed-article:2233709pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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