CHROMATIN RELAXATION BY OVEREXPRESSION OF MUTANT P53, HPV16-E6, OR CYCLIN-G TRANSGENES

In this study, using a cell line that carries endogenous wild-type p53 genes, we show that transfection of cells with mutant p53, HPV16-E6, or cyclin G transgenes results in the disruption of higher-order chrom atin structure, as evidenced by enhanced sensitivity to micrococcal nu clease. Multiple mechanisms may contribute to this phenotype, includin g histone H1 phosphorylation, direct binding of oncoproteins to nuclea r matrix attachment sites, and altered expression of component genes o f the p53 pathway, whose products may function in maintenance of chrom atin structure. (C) 1998 Academic Press.