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There are many examples within gene complexes of transcriptional enhancers interacting with only a subset of target promoters. A number of molecular mechanisms including promoter competition, insulators and chromatin looping are thought to play a role in regulating these interactions. At the  Drosophila  bithorax complex (BX-C), the IAB5 enhancer specifically drives gene expression only from the  Abdominal-B  ( Abd-B ) promoter, even though the enhancer and promoter are 55 kb apart and are separated by at least three insulators. In previous studies, we discovered that a 255 bp  cis -regulatory module, the promoter tethering element (PTE), located 5′ of the  Abd-B  transcriptional start site is able to tether IAB5 to the  Abd-B  promoter in transgenic embryo assays. In this study we examine the functional role of the PTE at the endogenous BX-C using transposon-mediated mutagenesis. Disruption of the PTE by  P  element insertion results in a loss of enhancer-directed  Abd-B  expression during embryonic development and a homeotic transformation of abdominal segments. A partial deletion of the PTE and neighboring upstream genomic sequences by imprecise excision of the  P  element also results in a similar loss of  Abd-B  expression in embryos. These results demonstrate that the PTE is an essential component of the regulatory network at the BX-C and is required  in vivo  to mediate specific long-range enhancer-promoter interactions.

Disruption of the Abdominal-B Promoter Tethering Element Results in a Loss of Long-Range Enhancer-Directed Hox Gene Expression in Drosophila