A hotspot for promoter-dependent recombination in polyomavirus DNA

We have engineered polyomavirus (Py) DNA molecules carrying two large direct repeats within the late coding region, as well as a deletion encompassing the TATA box in the early promoter. Such constructs recombine less readily than a construct containing the same duplication of late sequences, but an intact early promoter. Furthermore, residual recombination in the molecules with a deletion occurs between homologous sites which differ from those used in the molecule without deletion. These findings are consistent with recombination being stimulated by transcription originating from the early promoter, rather than facilitated by the "openness" of viral chromatin undergoing transcription.