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Nucleic Acids Research, 2003, Vol. 31, No. 10 2483-2494
© 2003 Oxford University Press

The capacity to form H-DNA cannot substitute for GAGA factor binding to a (CT)n·(GA)n regulatory site

Quinn Lu1, John M. Teare1, Howard Granok1,2, Marci J. Swede1, Jenny Xu1 and Sarah C. R. Elgin1,2

1 Department of Biology and 2 Division of Biology and Biomedical Sciences, Washington University, St Louis, MO 63130, USA

Jenny Xu, Merck Research Laboratory, West Point, PA 19486, USA

Previous studies of the Drosophila melanogaster hsp26 gene promoter have demonstrated the importance of a homopurine·homopyrimidine segment [primarily (CT)n·(GA)n] for chromatin structure formation and gene activation. (CT)n regions are known to bind GAGA factor, a dominant enhancer of PEV thought to play a role in generating an accessible chromatin structure. The (CT)n region can also form an H-DNA structure in vitro under acidic pH and negative supercoiling; a detailed map of that structure is reported here. To test whether the (CT)n sequence can function through H-DNA in vivo, we have analyzed a series of hsp26-lacZ transgenes with altered sequences in this region. The results indicate that a 25 bp mirror repeat within the homopurine·homopyrimidine region, while adequate for H-DNA formation, is neither necessary nor sufficient for positive regulation of hsp26 when GAGA factor-binding sites have been eliminated. The ability to form H-DNA cannot substitute for GAGA factor binding to the (CT)n sequence.


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