DNA polymerase β(pol β) is a constitutively expressed DNA repair enzyme in vertebrate cells. Yet, it had been shown previously that the pol β mRNA level increases in Chinese hamster ovary (CHO) cells within 4 h after treatment with several monofunctional DNA damaging agents, notably, N-methyl-N′-nitro-N-nitrosoguanidine (MNNG). Herein we report that a transfected pol β promoter fusion gene is activated by MNNG treatment of CHO cells; mRNA from the transfected gene is ≈ 10-fold higher in treated cells than in untreated cells 16 h after treatment. This activation is mediated through the decamicleotide palindromic element GTGACGTCAC at positions -49 to -40 in the "TATA-less" core promoter. This clement, which is similar to the ATF/CREB transcription factor-binding site in a number of mammalian genes, forms the center of a strong protein-binding site for CHO cell nuclear extract proteins. Mutated pol β promoter fusion genes lacking the element fail to bind protein at this site and fail to respond to MNNG treatment of cells.
|Original language||English (US)|
|Number of pages||5|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|State||Published - Jan 1 1991|
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