DNA rearrangement affecting expression of the BK virus transforming gene

Abstract

BK virus mutant pm-522, forming small turbid plaques on human cells, can transform rat or hamster cells much more efficiently than the wild-type BK virus (wt-501) does. We compared the nucleotide sequence of wt-501 HindIII C segment with that of pm-522 HindIII-C, which contains the mutation responsible for the altered plaque type and transforming capacity. The difference between the two BK viruses was the local DNA rearrangement (deletions and duplications) that had occurred in the putative control region for early transcription in pm-522 DNA. Whereas wt-501 had three sets of 68-base pair repeats (the central set had a deletion of 18 base pairs) in this region, pm-522 had one set of 68-base-pair units and two sets of shorter 37-base-pair repeats. Three BK virus mutants, forming clear large plaques like those of wt-501 but capable of transforming rat cells, were derived from the recombinant virus carrying the HindIII C segment of pm-522. These mutants had further duplications of short segments originating from the pm-522 sequence in the putative early control region.