Simian virus 40-mediated cis induction of the Xenopus beta-globin DNase I hypersensitive site.

Abstract

Regions in chromatin which are hypersensitive to the action of DNase I appear to be associated with sites of genetic activity; the association between DNase I hypersensitivity and transcriptional activation is well known. In the case of the chicken beta-globin gene the establishment of a DNase I hypersensitive site is dependent on tissue-specific trans-acting factors. Such factors have also been implicated in the action of viral and cellular enhancers, which are themselves hypersensitive to DNase I. Enhancers have been defined operationally as DNA sequences which act in cis to potentiate transcription from their own, heterologous or cryptic promoters. This activity is essentially unaffected by changes in the orientation, position (5' or 3') or distance of the enhancer element with respect to its cognate promoter. We demonstrate here that the transcriptional rescue of the Xenopus laevis beta-globin gene by simian virus 40 (SV40) sequences including the enhancer coincides with the conferment of DNase I hypersensitivity upon that gene, and that this occurs in the absence of any change in the complement of trans-acting factors. These results suggest that a propensity to form sites hypersensitive to the action of DNase I is encoded in the primary sequence of DNA, and that this predilection is aggravated by SV40 sequences, perhaps through a mechanism dependent on supercoiling.