Abstract
The mammalian DNA β-polymerase (β-pol) gene is constitutively expressed in cultured cells as a function of growth stage and DNA replication, but is expressed in rodents in a tissue-specific fashion. As revealed by transient expression experiments with wild-type and mutated β-pol promoter fusion genes, the cloned human β-pol promoter is transcriptionally regulated by signals acting through the single palindromic sequence (GTGACGTCAC) known as an ATF/CRE-binding site centered at position −45 in the core promoter. Although the mere presence of the ATF/CRE palindromic sequence in a promoter does not always confer cAMP responsiveness or protein binding over and around the ATF/CRE sequence, we find that agents that increase cAMP levels (forskolin and IBMX) in HeLa cells activate the β-pol promoter; activation also can be observed by coexpression of the protein kinase A catalytic subunit. Experiments with mutagenized β-pol promoters indicate that the ATF/CRE-binding site mediates these effects. Thus, the ATF/CRE-binding site in the context of this TATA-less constitutive promoter is able to respond to the kinase A signal transduction pathway.
Original language | English (US) |
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Pages (from-to) | 61-69 |
Number of pages | 9 |
Journal | DNA and Cell Biology |
Volume | 11 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1992 |
Externally published | Yes |
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cell Biology