The capacity to form H-DNA cannot substitute for GAGA factor binding to a (CT)n*(GA)n regulatory site
Originally Published In
Lu Q, Teare JM, Granok H, Swede MJ, Xu J, Elgin SC. The capacity to form H-DNA cannot substitute for GAGA factor binding to a (CT)n*(GA)n regulatory site. Nucleic Acids Res. 2003;31(10):2483–2494. doi:10.1093/nar/gkg369
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.
Lu, Quinn; Teare, John; Granok, Howard; Swede, Marci; Xu, Jenny; and Elgin, Sarah C.R., "The capacity to form H-DNA cannot substitute for GAGA factor binding to a (CT)n*(GA)n regulatory site" (2003). Biology Faculty Publications & Presentations. 203.
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