The transcriptionally active ev-3 and inactive ev-1 endogenous retrovirus loci in chick cells differ in that ev-3 is undermethylated, preferentially sensitive to DNase I digestion, and contains nuclease hypersensitive sites in each of its two long terminal repeats. Transient exposure of cells to 5-azacytidine, a cytosine analogue which cannot be methylated at the 5 position, results in the hypomethylation and transcriptional activation of ev-1, as well as the acquisition of at least one nuclease-hypersensitive site within the chromosomal domain of ev-1.
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